RRAD and cardiac hypertrophy: Studies on mice indicated that deficiency of RAD function in cardiomyocytes, which can lead to an increased L-type Ca2 + current (ICa–L) via upregulation of LTCC expression in the plasma membrane (Yada et al., 2007), significantly increased stress-induced cardiac hypertrophy and remodeling in vitro (Chang et al., 2007) and cardiac fibrosis in vivo (Zhang et al., 2011).