In the representative case of lung cancer cells (line A549), Lee et al. (2015) demonstrated that after 24 h of exposure to CAP (200 μM), a downregulation in the expression of tNOX ensued, followed by a drop in the NAD+/NADH intracellular ratio and consequent affectations in the expression and activity of SIRT1, whose derogation was succeeded by increases in both the acetylation (Lys382) and the phosphorylation (Ser46) of the tumor suppressor p53, leading to a significant increase in apoptotic activity in tumor cells. This evidence concerns the gene ENOX2 and lung carcinoma.