The discovery of serotonin was made in 1948 by Irvine Page, Maurice M. Rapport, and Arda Green, who never imagined the important biological roles that this fundamental molecule has in all living beings, from plants to animals and humans. The importance of serotonin in humans lies in the fact that alterations in its neurotransmission can produce various chronic or acute mental illnesses at the central nervous system level. This includes disruptions in its synthesis to its quantum release, the presence and type of receptors, the transporters' functionality, the presence of isoforms, and interactions with other neurotransmitters. Serotonin's participation has been demonstrated in conditions such as autism, schizophrenia, hyperactivity, depression, anxiety, obsessive-compulsive disorder, aggression, insomnia, and stress. This amazing discovery has significantly influenced the fields science, medicine, and researchers within the field of serotonin. Pathological conditions and experimental models in which 5-HT or closely related molecules have been pharmacologically modulated suggest that 5-HT concentration must remain within normal ranges for proper brain function. The versatility of 5-HT is evident in its capacity to produce a range of physiological effect, sometimes even opposing ones, are determined by the receptor subtypes it interacts with and the intracellular signalling pathways coupled to them. Among these, the 5-HT2A receptor is a component of the serotonin system deeply implicated in effects related to psychosis and memory deficits. This intricate involvement poses a significant challenge to unravel its role in patients suffering from these conditions. In a recent bibliometric analysis of schizophrenia and serotonin, we promoted the practical concept of serotoninomics, whose purpose is to find precise answers to basic, clinical, translational, medical, and clinical pharmacological research questions on serotonin.Schizophrenia is a chronic and complicated psychiatric and psychological illness. It is characterised by a set of symptoms that include hallucinations, delusions, speech or behavioural disorders, emotional blunting, anhedonia, alogia, apathy, and other defective cognitive abilities. Schizophrenia is a devastating developmental disorder that arises from the interaction between genetic and environmental factors (1). Several lines of evidence suggest that the serotonergic system plays a critical role in the pathogenesis of schizophrenia in at least a subpopulation of patients. According to the neuropathological changes, this heterogeneous condition has been divided into three main domains: positive symptoms, negative symptoms, and cognitive dysfunction. Additionally, some researchers have conceptualised schizophrenia as a disease of functional "dysconnectivity" (2)(3)(4) or "synapse disorder" (5,6), affecting the serotonin quantum release machinery within the synapse during its synthesis, its interaction with its receptors, or its correlation with other neurotransmitters (i.e. dopamine, glutamate, GABA) (7,8). Acute relapses of this disease are characterised by the exacerbation of positive psychotic symptoms, while chronic disabilities occur due to cognitive causes and negative symptoms (apathy and social withdrawal) (9). The disease profoundly affects not only the individuals who suffer from it but also their families and caregivers, typically manifesting during late adolescence or early adulthood. (1,9).Because the condition is so heterogeneous, the presence of symptoms from these domains in the disease makes its diagnosis and treatment difficult. The development of some mental diseases, including schizophrenia, are marked by subtle molecular, heritable, and epigenetic changes, which initiate a cascade of events within individual cells before overt signs and symptoms manifest themselves. These events include effective quantum release; appropriate signalling by receptors and activation by second messengers; the functionality of transporters; the ability to take up, store, and release serotonin; the presence of isoforms; the activity of tryptophan hydroxylase-2 (TPH2; lack of activity); the availability of the amino acid L-tryptophan (L-Trp); deviation towards other pathways of its metabolism how to as the kynurenine-like pathway; mutations; and other dysfunctions. Therefore, individuals with schizophrenic parents or siblings will have a higher risk of developing the disease due to this hereditary component (between 8% and 12%; (10). The most common theory regarding the neurobiology of schizophrenia is a chemical imbalance in the brain, marked by deregulation of the mesolimbic pathway as a result of dopaminergic hyperactivity and, in some cases, alterations in the serotonergic system in specific nuclei of the brain (prefrontal cortex, temporal cortex, thalamus, hypothalamus, and basal ganglia) or in the interaction between dopamine and serotonin (9).Serotonin is a molecule with numerous functions within the central nervous system (CNS), which is why it plays an essential role in the delicate balance of neuronal function. Alterations in serotonin concentration can contribute to the onset of schizophrenia, and conversely, schizophrenia can gradually affect the serotonergic systems of the brain (11). As the initial molecular and genetic changes progress, often silently and insidiously, these molecular perturbations extend to higher organisational levels: tissues, organs, and systems. In this way, all of these changes will culminate in dysregulations that will contribute to the characteristic symptoms of schizophrenia (i.e. altered perception) (12). A key limitation in the study of schizophrenia is that it is difficult to conclusively determine causation, given the interactive influences exerted by the different molecular and physiological mechanisms involved (9,11,12). Therefore, the understanding of these early molecular events is essential for unravelling schizophrenia's...