The balance between acetylation by lysine acetyltransferase (KAT9, which inhibits G6PD activity), and deacetylation by SIRT2 (which reactivates G6PD) controls PPP flux and the production of cytosolic NADPH, which is essential for redox homeostasis and cancer cell survival under oxidative stress [31,32,33]. The gene discussed is G6PD; the disease is cancer.