also found that GLUD1 was acetylated at K191, K390, K457, K489, and K527 and all the acetylation levels were downregulated in tumor tissues,7 which is consistent with our data (Table S6) ADH1B is a disease‐associated protein of alcohol dependence and fetal alcohol syndrome,61 which catalyzes the NAD‐dependent oxidation of all‐trans‐retinol and its derivatives involved in retinoid metabolism.58, 62. The gene discussed is ADH1B; the disease is alcohol dependence.