The mechanism underlying this event involves GSK-3β activation in TGNs, likely in association with the inactivation of the PI3K/Akt pathway, while inhibition of GSK-3β effectively blocked SNAP-induced expression and production of CGRP and other migraine-related factors (e.g., SP, CCK, and PEG2; Figure 5E). This evidence concerns the gene AKT1 and migraine disorder.