As tight control of CaV1.2 activity during EC-coupling is essential and deregulated CaV1.2 function has been shown in a multitude of different CVDs, e.g., hypertension, cardiac arrhythmia and heart failure, specific targeting of PP-CaV1.2 interactions might be a versatile drug targeting in the future (Splawski et al., 2004; Tang et al., 2008; Domes et al., 2011; Hong et al., 2012; Tajada et al., 2013). This evidence concerns the gene CACNA1C and heart failure.