The possible mechanism is that cADPR, the main hydrolysate of CD38, induces the opening of the iron channel of TRPM2, leading to intracellular Ca2+ influx, which then leads to increased Nuclear Factor erythroid 2-Related Factor 2 (NRF2) level and decreases Kelch-like ECH associated protein-1 (KEAP-1) expression in lung cancer, thus accelerating tumor progression. The gene discussed is CD38; the disease is neoplasm.