CACNA1C and diabetes mellitus: Findings indicating that hyperphosphorylation of CaV1.2 at S1928 underlies L-type Ca2+ channel potentiation during hyperglycemia and diabetes also open new possibilities to develop improved Ca2+ channel blockers that correct impaired channel function (e.g. prevent S1928 hyperphosphorylation), as opposed to established therapies that aim to reduce Ca2+ influx.