TRPM2 controlled autophagy by an mTOR (mammalian target of rapamycin) independently but JNK (Jun N-terminal Kinase) signaling reliant pathway, facilitated through regulation of ATGs, BNIP3 as well as JNK stimulation. Apoptotic properties of together paclitaxel and doxorubicin were higher in TRPM2 exhausted cells, indicating that TRPM2 conserves the survival of cells where inhibition raises sensitivities of chemotherapy and proposing this as a therapeutic attitude to increase the cell death of gastric tumors. The gene discussed is MAPK8; the disease is gastric neoplasm.