CAMK2D and familial dilated cardiomyopathy: However, the heterozygous or homozygous Rbm20ΔRRM mice did not show any significant differences in cardiac chamber geometry and dimensions compared to wild-type controls (Methawasin et al., 2014), suggesting that switching of the titin isoforms to N2BA-G together with the splicing change in Camk2d and Ldb3 per se does not cause DCM-like phenotypes such as LV chamber dilatation and systolic dysfunction.