RBM20 and familial dilated cardiomyopathy: Although multiple mechanisms may account for the dysregulated post-transcriptional activity of mutant RBM20 proteins, it is particularly interesting that correcting these pathogenic variants through precise base editing or promoting the interaction of RBM20 with its nuclear importer can redirect RBM20 nuclear localization and rescue DCM, at least in animal models [27,28,40].