Genetic mitochondrial cardiomyopathies firmly establish causality, as mtDNA point mutations (e.g., m.3243A > G), defects in mtDNA maintenance (TK2, POLG), and TAFAZZIN-related cardiolipin remodeling produce cardiomyopathy phenotypes, highlighting opportunities for precision therapies such as metabolic modulation, nucleoside supplementation, or cardiolipin stabilization [29,84,85,86,87,88]. The gene discussed is POLG; the disease is cardiomyopathy.