This is because (1) LGI1 was shown to be enriched at the AIS and colocalized with ADAM22 and Kv1 channels where they likely form higher-order clusters and regulate the density of Kv1 channels,18,37 (2) epilepsy-associated sequence variations of LGI1 led to impaired trafficking and anchoring at the AIS,19 and (3) our experimental and modeling results suggested an impaired Kv1-channel activity in LRR-mAb–treated neurons (Figures 2–4). The gene discussed is ADAM22; the disease is epilepsy.