FCGR1A encodes the high-affinity IgG receptor CD64, expressed on antigen-presenting cells, mediating ADCP, ADCC, and immune complex clearance, thus bridging innate and adaptive immunity. Recent studies show FCGR1A overexpression in various cancers, including ovarian, cervical, renal, and melanoma, where it promotes migration, invasion, and EMT via LSP1 regulation, correlating with advanced stage, lymph node metastasis, and poor prognosis. In rheumatoid arthritis, monocytic FCGR1A upregulation correlates with disease activity; genetic variants affect CD64 phagocytosis and cytokine production, associating with sarcoidosis susceptibility and severity. Collectively, FCGR1A overexpression plays pivotal roles in tumor progression and immunoinflammation, positioning it as a potential diagnostic, prognostic, and immunotherapeutic target.