Gating changes permitting enhanced Ca2+ inward current through Cav1.3 were not only identified as cause for excessive aldosterone secretion in adrenal adenomas (Azizan et al., 2013) but also as cause for PASNA, a severe human congenital disease (Scholl et al., 2013) and as high risk de novo mutations for autism with intellectual disability (Pinggera et al., 2015). Here, CACNA1D is linked to aldosterone-producing adenoma with seizures and neurological abnormalities.