RBM20 and familial dilated cardiomyopathy: Pathogenic RBM20 variants resulting in loss-of-function lead to missplicing of sarcomeric and calcium-handling genes, implicated in DCM (TTN missplicing considered to be the major contributing mechanism), and are associated with an aggressive early-onset phenotype with an increased predilection to cardiac transplantation, severe arrhythmia and SCD [114,115,116].