Defects in thin filament length underlie disease progression in LMOD2-KO neonatal mice [4,5] and LMOD2-related neonatal cardiomyopathy reported in humans [8,9,10,11]; yet, LMOD2 has been listed in few cardiomyopathy panels with inconsistent indications for testing, e.g., “familial dilated cardiomyopathy” [12,13], “congenital structural myopathy” [14], and “hypertrophic cardiomyopathy” [15]. Here, LMOD2 is linked to congenital structural myopathy.