Human mutations in the gating brake are associated with arrhythmic vulnerabilities such as epilepsy (27, 28) or autism spectrum disorder (78), and it is the platform where Ca2+ and CaM can modulate the low-voltage gating behavior in T-type channels, in a manner that is unique from the regulation of CaM universally at the IQ motif in the C-terminal tails of Cav1 and Cav2 calcium channels (1, –, 5) and Nav1 sodium channels (6). This evidence concerns the gene CALM1 and autism spectrum disorder.