Background: Interindividual variability in response to anti-inflammatory therapies remains a major challenge in clinical practice. Nonsteroidal anti-inflammatory drugs, corticosteroids, and biologic agents are widely used in adult and pediatric inflammatory diseases, but their efficacy and safety are influenced by pharmacokinetic, pharmacodynamic, developmental, and genetic factors. Methods: A structured literature review was conducted in PubMed and Embase for English-language publica-tions from January 2000 to January 2026. Clinical studies, trials, observational studies, systematic reviews, meta-analyses, guidelines, and relevant reviews were analyzed, with emphasis on phar-macogenomic determinants of response and toxicity. Results: The strongest actionable evidence concerns CYP2C9 variants affecting the metabolism of several nonsteroidal anti-inflammatory drugs, including ibuprofen, celecoxib, meloxicam, and related agents. Reduced-function alleles are associated with decreased clearance, increased drug exposure, and higher risk of dose-related ad-verse events. For corticosteroids, variants in NR3C1, FKBP5, STIP1, GLCCI1, and pharmacokinetic genes may contribute to variability in responsiveness and toxicity, although clinical implementation remains limited. For biologics, HLA-DQA1*05 is a reproducible predictor of anti-drug antibody formation and secondary non-response to anti-TNF therapy. Conclusion: Pharmacogenomics offers a promising strategy to personalize anti-inflammatory therapy. While CYP2C9-guided nonsteroidal anti-inflammatory drug prescribing is currently the most clinically actionable application, further prospective and pediatric-specific studies are needed to support broader implementation.