During the process of brain development, excessive activation of the mTOR signaling cascade can disrupt the maturation and migration of neurons, leading to abnormal enlargement of neuronal cells and the formation of dysmorphic neurons, which are characterized by FCD II.[7] It has been demonstrated that the dysregulation of the mTOR signaling pathway is associated with FCD II in ≈15.6% of patients.[7, 8] Nevertheless, the molecular pathogenesis of the predominant cohort of FCD patients remains elusive. Here, MTOR is linked to fleck corneal dystrophy.