Conversely, mutations in the LMNA gene (lamin A/C, representing 5–6% of genetic DCM) (Hasselberg et al., 2018), FLNC (filamin C) (Ortiz-Genga et al., 2016), DES (desmin) (Capetanaki et al., 2015), PLN (phospholamban) (Schmitt et al., 2003), SCN5A (McNair et al., 2011), and mutations of RBM20, the regulator of TTN splicing (Refaat et al., 2012), have been identified as malignant causes of DCM, featuring a marked arrhythmic propensity in patients. This evidence concerns the gene RBM20 and familial dilated cardiomyopathy.