ATP5F1C encodes the gamma subunit of mitochondrial ATP synthase (Complex V), a critical component of the F1 catalytic head domain. This subunit functions as part of the rotational mechanism that couples proton translocation across the inner mitochondrial membrane to ATP synthesis from ADP 1. The gamma subunit works with the central stalk to enable the rotary catalysis essential for oxidative phosphorylation, and is necessary for F1 assembly intermediate formation 12. ATP5F1C expression correlates with cellular ATP production capacity and mitochondrial function. Dysregulation of ATP5F1C is implicated in multiple pathological conditions: in diabetic kidney disease, Rheb1 deficiency increases ATP5F1C acetylation, impairing mitochondrial ATP production and accelerating podocyte senescence 3. In cancer, ATP5F1C overexpression marks metastatic cells with enhanced ATP production, proliferation, and stemness; ATP5F1C knockdown or targeting with bedaquiline reduces metastatic capacity 4. Additionally, ATP5F1C is involved in magnesium-ATP formation and serum magnesium homeostasis in type 2 diabetes 5. ATP5F1C expression is also upregulated during COVID-19 infection as a compensatory response to viral-induced mitochondrial dysfunction 6. These findings establish ATP5F1C as a therapeutic target in metabolic disease, cancer, and viral infection.