CACNA1A and Cerebellar atrophy: This effect, in combination with ΔF1502-induced changes in the kinetics of activation, deactivation and inactivation of CaV2.1 channels, allow significantly higher Ca2+ influx in response to stimuli of physiological traits, and support the causative role of ΔF1502 (and, by extension, of other gain-of-function CaV2.1 mutations) in congenital ataxia and/or cerebellar atrophy.