Notably, while mutations in TPM1 (encoding the α-tropomyosin chain) have been well-established in hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM) (Rivenes et al., 2000; Lipshultz et al., 2019), definitive pathogenic evidence linking it to RCM remains exceptionally rare, and the specific molecular mechanisms are unclear. The gene discussed is TPM1; the disease is familial dilated cardiomyopathy.