Because tumor-infiltrating T cells in PPARGC1A mutation carriers experience PPARGC1A inhibition and T cell exhaustion due to metabolic insufficiency [42], BRCA1/2-mutant cancer cells in PPARGC1A mutation carriers have an advantage in escaping immune surveillance and thus can develop into tumors earlier than in individuals without PPARGC1A mutations. The gene discussed is PPARGC1A; the disease is neoplasm.