In contrast, depletion of DiPRO1 in cancer cells induced activation of signaling pathways for inflammation (TNF/TNFR1/2, inflammasome, neuroinflammation), stress response (MAPK signaling), and apoptosis (intrinsic pathway, apoptotic execution, and HIV1 induction of apoptosis). This evidence concerns the gene TNFRSF1A and cancer.