CACNA1C and schizophrenia: Expression studies in cell lines and postmortem tissue have suggested that the intron 3 risk variants may act to decrease expression of CACNA1C, although the exact direction of effect has varied between studies and tissue types.8–12 Rare deleterious mutations in VGCCs have also been found to be associated with risk for schizophrenia.13 Notably, this enrichment was primarily driven by pore-forming alpha-1 subunits and alpha-2-delta auxiliary subunits of VGCCs, including deleterious mutation loss of function variants in CACNA1C.13