FLNC encodes filamin C, a muscle-specific actin-binding protein critical for sarcomere assembly and organization 1. It functions as a large actin-cross-linking protein essential for structural integrity at Z-lines and plays a central role in maintaining sarcomere stability 2. FLNC participates in reorganizing the actin cytoskeleton in response to signaling events and is crucial for both structural integrity and cell signaling of the sarcomere 3. FLNC mutations cause diverse muscle and cardiac phenotypes through distinct pathomechanisms. Truncating variants cause haploinsufficiency leading to dilated cardiomyopathy (DCM) and arrhythmogenic cardiomyopathy with high sudden cardiac death risk 34. Non-truncating missense variants, predominantly in the ROD2 domain, cause protein aggregation resulting in hypertrophic cardiomyopathy and myofibrillar myopathy 32. FLNC is classified as having definitive evidence for DCM pathogenicity 5 and is among the more prevalent genetic causes of inherited DCM 3. Additionally, FLNC variants cause distal myopathies with progressive muscle weakness in hands and feet 6. Genotype-based risk stratification using FLNC variants predicts sudden cardiac death risk more precisely than phenotype-based classification 7, emphasizing the importance of molecular diagnosis for clinical management and prognostication.