For instance, the overexpression of CD38 in several solid and hematological tumors can lead to growth and metastatic dissemination through any of the following redundant effects: (i) decline in NAD+ levels, both intracellular and extracellular [89,90,91,92]; (ii) hypertrophy of the alternative adenosinergic pathway in the TME and especially in tumor cells, with consequent weakening or suppression of CD8+ T cell function; (iii) [Ca2+]i-related mechanisms of cADPR in tumor cells, including the downregulation of the tumor suppressor KEAP1 and parallel upregulation of the NRF2 oncogene [93]. This evidence concerns the gene KEAP1 and neoplasm.