However, the reports on DCA and UDCA are contradictory [7, 258, 262–264] in physiological concentrations, LCA tunes cancer cell metabolism towards a more oxidative state (through AMP-activated protein kinase (AMPK), PGC-1β and NRF1/NFE2L1) and induces mild oxidative stress through reducing NRF2 (nuclear factor erythroid 2-related factor 2, NFE2L2) expression and inducing Inducible nitric oxide synthase (iNOS) that reverts EMT, reduces VEGF expression, induces antitumor immunity and changes to cancer metabolism that culminates in reduced metastasis formation [7, 11]. The gene discussed is NRF1; the disease is cancer.