CACNA1D and primary aldosteronism: To prove this hypothesis more patients need to be identified with either PASNA, ASD with or without seizures or primary aldosteronism and strongly gating modifying de novo germline mutations in CACNA1D. If this is the case and the corresponding mutations (like G407R, A749G) retain their sensitivity to brain‐permeant L‐type Ca2+ channel blockers (such as isradipine, nifedipine or nimodipine), experimental therapies with these drugs in affected patients would be justified.