Furthermore, at the biochemical level, it was identified that cADPR, a primary hydrolytic product of CD38, induced the opening of TRPM2 iron channels, resulting in intracellular Ca2+ influx and subsequent upregulation of NRF2 levels while downregulating KEAP1 expression in NSCLC cells (20). The gene discussed is TRPM2; the disease is non-small cell lung carcinoma.