Elevated in cancers, K235 acetylation of ALKBH5 contributes to tumorigenesis, revealing a targetable mechanism in cancer therapy.[116] In addition, SIRT1‐mediated deacetylation of IGF2BP2 regulates its interaction with the ATP6V1A mRNA, influencing RNA stability and cellular lysosomal function. The gene discussed is ATP6V1A; the disease is cancer.