ATP6V0A1 and schizophrenia: If this interaction is present in cerebellar neurons, this evidence could either suggest that the upregulation of calmodulin in the cerebellum in suicide schizophrenia subjects could be a mechanism to compensate for the possible lower abundance of calmodulin at the synapses due to a reduction in VPP1 levels or that it could be a compensatory mechanism for the lower formation/release of synaptic vesicles [37,66].