Interestingly, the hyperactivation of CaV1.2 LTCCs by CaMK-II is implicated in Timothy Syndrome, a multiorgan human genetic disorder whose symptoms include mental retardation and cardiac disease [55,56], and the excessive activation of CaV1.3 LTCCs is implicated in the loss of dendritic spines following dopamine depletion in animal models of parkinsonism [57]. This evidence concerns the gene CACNA1C and hereditary disease.