CACNA1C and cardiac hypertrophy: In contrast, with cardiac-specific overexpression of CBD−REM or a caveolae−targeted CaV1.2 activator (CBD−β2a, a mutated β2aC3S/C4S fused C−terminal to CBD) in mice, both transgenic mice with pressure overload-induced cardiac hypertrophy did not display significant changes in cardiac function compared to wild-type mice (Figure 3) although CBD−β2a potentiated the NFAT translocation in feline cardiomyocytes (74).