Acne vulgaris is a widespread dermatological condition that significantly affects the quality of life of adolescents and adults. Traditionally, acne pathogenesis has been linked to factors such as excess sebum production, follicular hyperkeratinization, and the presence of Cutibacterium acnes (C. acnes). However, recent studies have highlighted the role of the skin microbiome, shifting focus from individual pathogens to microbial community dynamics. This review critically evaluates existing research on the skin microbiome and its relationship to acne, focusing on microbial diversity, C. acnes strain variability, and emerging therapies targeting the microbiome. While certain studies associate C. acnes with acne severity, others show this bacterium’s presence in healthy skin, suggesting that strain-specific differences and overall microbial balance play crucial roles. Emerging therapeutic approaches, such as probiotics and bacteriophage therapy, aim to restore microbial equilibrium or selectively target pathogenic strains without disturbing the broader microbiome. However, the lack of standardized methodologies, limited longitudinal studies, and the narrow focus on bacterial communities are major limitations in current research. Future research should explore the broader skin microbiome, including fungi and viruses, use consistent methodologies, and focus on longitudinal studies to better understand microbial fluctuations over time. Addressing these gaps will enable the development of more effective microbiome-based treatments for acne. In conclusion, while microbiome-targeted therapies hold promise, further investigation is needed to validate their efficacy and safety, paving the way for innovative, personalized acne management strategies.

Immune checkpoint inhibitors (ICIs) have transformed the treatment of multiple malignancies, yet durable clinical responses remain limited to a subset of patients. Accumulating evidence identifies the gut microbiome as a regulator of antitumour immunity that can influence treatment efficacy and toxicity through microbial metabolism, epithelial barrier integrity, inflammatory signalling, and host immune responses. This review critically evaluates the microbiome as both a predictive biomarker and therapeutic target in precision oncology. It moves beyond descriptive taxonomic associations by assessing emerging functional and mechanistic models that integrate microbial metabolites, ecological interactions, strain-level variation, and host–microbiome communication. Clinical and translational evidence from melanoma, non-small cell lung cancer, colorectal cancer, hepatocellular carcinoma, renal cell carcinoma, and urothelial carcinoma reveals marked differences in the reproducibility and clinical maturity of reported microbial signatures. Emerging microbiome-targeted strategies, including dietary modulation, faecal microbiota transplantation (FMT), live biotherapeutic products (LBPs), and defined microbial consortia, may enhance ICI responsiveness, with responder-derived FMT providing important early clinical proof of concept. However, inter-individual variability, donor–recipient compatibility, microbial engraftment, the lack of standardised analytical approaches, and unresolved safety and regulatory requirements continue to limit clinical translation. Pending prospective validation, reasonable clinical practice is to avoid unnecessary microbiome-disrupting antibiotics, systematically document diet and concomitant medications, evaluate FMT and LBPs within regulated clinical trials, and interpret microbiome profiles alongside established tumour and host biomarkers rather than as stand-alone tests. Current evidence therefore supports a cautious shift towards functional microbiome-guided precision oncology, providing a foundation for personalised strategies to improve cancer immunotherapy outcomes.