This thesis focuses on the role of apoptosis, or programmed cell death, in the pathogenesis and treatment of inflammatory diseases. It analyses how dysregulated apoptosis contributes to disorders such as rheumatoid arthritis, Hashimoto’s thyroiditis, systemic sclerosis, and diabetes mellitus. Current therapies largely focus on symptom management, but the work highlights emerging strategies targeting apoptosis-related molecules to achieve disease modification. In rheumatoid arthritis, selective induction of apoptosis in fibroblast-like synoviocytes and pro-inflammatory immune cells is proposed, using pathways like p53, NF-κB, and Bcl-2, as well as biologics and nanomedicine. For Hashimoto’s thyroiditis, molecular therapies, antioxidants, and stem cell approaches could preserve thyroid epithelium. In systemic sclerosis, balancing pro- and anti-apoptotic signals through microRNAs and anti-IL-6 therapy may limit fibrosis. For diabetes, protecting pancreatic β-cells and kidneys by modulating caspases, oxidative stress, and ER stress is emphasized. Overall, apoptosis-targeted therapies hold promise for precise, effective, and less toxic treatments .