Also, Hartung et al. [8] stated that in AE, particularly with leucine-rich glioma-inactivated 1 (LGI1), contactin-associated protein-like 2 (CASPR2), or glutamic acid decarboxylase (GAD) antibodies, patients frequently exhibit unilateral or bilateral T2/FLAIR hyperintensities in the medial temporal lobe, which can progress to hippocampal atrophy. The gene discussed is CNTNAP2; the disease is hippocampal atrophy.