Although chronic ER stress may result in YAP/TAZ exiting from the nucleus into the cytoplasm [24], our findings suggest that control of both intracellular TRAIL-R2/DR5 clustering and cFLIP expression by the YAP/TAZ-TEAD signaling module could represent a key event in the adaptive response of tumor cells to various types of inherent stress, that would otherwise ultimately lead to endoplasmic reticulum stress-induced apoptosis. Here, YAP1 is linked to neoplasm.