These results suggest that in FCD type II brain tissue lesions, the somatic variant of the RALA gene is primarily distributed in BCs and DNs, and this variant leads to the functional gain of RalA, activating its downstream effector molecules, further activating the PI3K-AKT-mTOR pathway, thus affecting neuronal migration, and ultimately leading to the development of FCD. This evidence concerns the gene AKT1 and fleck corneal dystrophy.