Rheumatoid arthritis (RA) is considered a chronic systemic, multi-factorial, inflammatory, and progressive autoimmune disease affecting many people worldwide. While patients show very individual courses of disease, with RA focusing on the musculoskeletal system, joints are often severely affected, leading to local inflammation, cartilage destruction, and bone erosion. To prevent joint damage and physical disability as one of many symptoms of RA, early diagnosis is critical. Auto-antibodies play a pivotal clinical role in patients with systemic RA. As biomarkers, they could help to make a more efficient diagnosis, prognosis, and treatment decision. Besides auto-antibodies, several other factors are involved in the progression of RA, such as epigenetic alterations, post-translational modifications, glycosylation, autophagy, and T-cells. Understanding the interplay between these factors would contribute to a deeper insight into the causes, mechanisms, progression, and treatment of the disease. In this review, the latest RA research findings are discussed to better understand the pathogenesis, and finally, treatment strategies for RA therapy are presented, including both conventional approaches and new methods that have been developed in recent years or are currently under investigation.

It is amazing to know that around 99.9% of the individuals genome among persons is alike, and only 0.1% of it differs in chromosome. This variance is accountable for the diversity in phenotypes and receptiveness of them to environmental effects. DNA variants are happening in numerous formulas. Mutations might be definite as order variants which happen in less than 1% of the populace, whereas the extra prevalent variant is identified as polymorphisms. More than 1% of the greatest public hereditary variants are known as single nucleotide polymorphisms (SNPs). In human genome, SNPs considered as plentiful figure of genetic variation, and their importance in contribution to many disease, drug efficacy, and side effects in addition to may represent a prophylaxis. SNPs represent a specific location at which more than one nucleotide is established and only two alleles at a SNP locus. More than 100 million SNPs have been recognized in human, in average each 300 nucleotide on usual. The gene which has more than one allele is a normal result of SNP. SNPs are not restricted to coding sequence, but may be associated with non-coding region. Many techniques are used to analyze SNPs and involve two phases, one for allele recognition and another for detection.

Acute Lymphoblastic Leukemia (ALL) is a heterogeneous blood cancer characterized by the uncontrolled growth of immature lymphoid cells due to dysregulated signaling pathways. It is the most common pediatric cancer, with high cure rates in children, but significantly lower survival rates in adults. Current theranostic strategies, including chemotherapy, immunotherapy, and nanomedicine, aim to improve detection and treatment precision but are limited by side effects, drug resistance, high costs, and stability issues. Notably, extracellular vesicles (EVs) offer a promising alternative, addressing these limitations through their natural biocompatibility and targeted delivery capabilities. EVs play a dual role in ALL: they contribute to leukemia progression by promoting tumor growth, immune suppression, and drug resistance via the transfer of oncogenic molecules, while also serving as valuable non-invasive biomarkers due to their specific miRNA and protein content. Their ability to deliver therapeutic agents directly to leukemic cells, combined with their stability and low immunogenicity, makes EVs a compelling tool for improving ALL treatments. Indeed, by targeting the molecular pathways influenced by EVs or leveraging them for drug delivery, innovative therapeutic strategies can be developed to enhance treatment outcomes and reduce side effects. Thus, EVs represent a promising frontier for advancing theranostic strategies in ALL, offering new opportunities to improve diagnosis and treatment while overcoming the limitations of traditional therapies. This review will explore the dual roles of EVs in ALL, addressing their contributions to disease progression and their potential as therapeutic agents and biomarkers for early diagnosis and targeted therapies.