Recent evidence suggests that FCD arises from de novo somatic mutations during brain development; most of these mutations have been identified in genes encoding regulatory proteins within the mechanistic target of rapamycin (mTOR) pathway, suggesting that aberrant mTOR pathway signaling is a critical mechanism accounting for the histopathological features of some FCD subtypes [1,2,10]. This evidence concerns the gene MTOR and fleck corneal dystrophy.