A similar mechanism has been shown to originate by pseudohypoxia as driven by VHL mutations in RCC cells, resulting in accrued autophagic flux via the endothelial PAS domain protein 1 (EPAS1)-dependent upregulation of inositol 1,4,5-trisphosphate receptor type 1 (ITPR1) [89]. Here, EPAS1 is linked to renal cell carcinoma.