Since increased KV2.1–CaV1.2 interactions play a major role in CaV1.2 clustering (Fig. 4) and in localized Ca2+ activity at KV2.1-forming ER–PM MCSs (Fig. 8), we predicted that KV2-dependent interactions with CaV1 may underlie elevations in Ca2+Mito in NPC disease. This evidence concerns the gene CAV1 and nasopharyngeal carcinoma.