In addition, it appears this fundamental function of the ESCRT-III pathway is “overactive”, hastening POM121 turnover in sALS iPSNs (Figs. 1 and 4) thereby giving rise to NPC pathology observed in disease [22, 23], a process once again slowed by reduction of either CHMP7 or CHMP2B (Figs. 1 and 4). Here, POM121 is linked to nasopharyngeal carcinoma.