This research article analysed how hormone-induced femoral head necrosis (FHN) affects “inflammatory pathways,” “apoptosis,” and “autophagy” in “Genetic Susceptibility” using molecular analysis and quantitative clinical risk factor assessment. Corticosteroids were supposed to cause FHN which is “Hormone-Induced,” but the fact that different people on the same hormone therapy felt sick at various periods showed the role of genetic predisposition in cellular susceptibility. “Osteocyte mortality,” “vascular impairment,” glucocorticoid-induced cellular responses and structural femoral head deterioration were thoroughly studied. Apoptosis, autophagy, and inflammatory signalling genes were studied in depth. The research article contained experimental, molecular and statistical techniques and used a retrospective cohort design involving many centres. A total of 1,239 eligible individuals met the inclusion criteria and were regarded as the final sample size. To evaluate the connection between genetic susceptibility and pathogenic pathway activity, biomarker profiles, imaging data, and sophisticated statistical models were employed. The ANOVA findings demonstrated a significantly correlated relationship between genetic susceptibility and cellular pathway disruption, demonstrating strong statistical significance. Compared to those with lower-risk profiles, patients with high-risk genetic susceptibility showed significantly enhanced inflammatory signalling, altered autophagic flux, and apoptotic activity. These data provide light on the mechanisms behind the observed clinical variability in glucocorticoid users. The biological reaction to hormone exposure was shown to be significantly influenced by genetic susceptibility, which exacerbated the pathogenic cascades leading to FHN. There needed to be an early warning system and effective patient care methods for those who were genetically prone to hormone-induced FHN.