Indeed, against the old hypothesis that PACAP and CGRP pathways are converging through the cAMP in the opening of adenosine triphosphate-sensitive potassium (KATP) channels, recent observation supports that PACAP38-induced hypersensitivity is not mediated via an increase in CGRP release, clearly highlighting the PACAP38 pathway as distinct from other migraine-provoking pathways, such as CGRP and the glyceryl trinitrate (the latter well-known as a CGRP-related) migraine trigger. The gene discussed is ADCYAP1; the disease is migraine disorder.