In dB/dB and HFD models of diabetes, the increase in L-type Ca2+ channel activity in cerebral vascular smooth muscle cells was attributed to activation of an unexpected AKAP5-anchored PKA signaling pathway leading to phosphorylation of the CaV1.2 subunit at S1928 (Fig. 2) [31, 112]. This evidence concerns the gene AKAP5 and diabetes mellitus.