Moreover, elevated activity and permeability of lysosomes has been noted in PDACs,[33] and our study suggests a mechanism to explain TFEB nuclear localization despite nutrient‐replete and mTOR‐active conditions.[23] Indeed, oncogenic signals might take advantage of involvement of FLCN‐FNIPs membrane sequestration in endolysosomal stress setting to drive TFEB‐dependent tumor growth. Here, FLCN is linked to neoplasm.