These findings indicate that CaM antagonists (e.g., W7 and CaM inhibitory peptide), activators of protein kinase Cα, or a specific Cav1.2 channel mutation (associated with Timothy syndrome) that moves CaM away from the IQ domain in the C-terminal tail of the channel promoted coupled gating between Cav1.2 channels [220]. The gene discussed is CACNA1C; the disease is Timothy syndrome.