While cancers derived from tissues with normal NAPRT levels are entirely dependent on the NAD+ salvage pathway for survival.408 Both the upregulated NAPRT in ovarian cancer and the high expression of NAMPT in glioblastoma, colorectal cancer tumors, and breast cancer, increase intracellular NAD+ levels, contributing to cancer cell metabolism and DNA repair process in tumors.409 Moreover, resistant CCRF-CEM cells with high QPRT activity exploit amino acid catabolism as a substitute pathway for NAD+ generation.410. The gene discussed is NAPRT; the disease is colorectal cancer.