TNNC1 encodes troponin C1, a core regulatory protein of striated muscle contraction that mediates calcium-dependent control of actin-myosin interactions. TNNC1 functions as part of the troponin complex alongside troponin I and troponin T, with calcium binding to TNNC1 abolishing the inhibitory action of troponin on actin filaments, thereby enabling muscle contraction. This mechanism applies to both cardiac and slow skeletal muscle, where TNNC1 regulates muscle filament sliding and contractile force generation. Clinically, TNNC1 has established disease relevance in cardiomyopathies. Among dilated cardiomyopathy (DCM) genes, TNNC1 variants were significantly enriched in specific patient subsets and contributed to approximately 17-26% of cases depending on cohort composition 1. TNNC1 was classified as having definitive evidence for DCM causation 2. For hypertrophic cardiomyopathy (HCM), TNNC1 initially had moderate evidence 3 but was recently upgraded to definitive status as a sarcomere gene 45. TNNC1 variants have also been identified in severe childhood-onset cardiomyopathies, supporting its critical role in early cardiac development and function 6. These findings establish TNNC1 as a high-evidence disease gene with clear diagnostic value in genetic testing for both DCM and HCM, particularly in familial and early-onset presentations.