With advancing age, p16+ cells accumulate in multiple tissues, where they are generally associated with tissue dysfunction, chronic inflammation, and various age‐related pathologies.[26] For example, senescent hepatocytes display impaired fatty acid oxidation, contributing to hepatic lipid accumulation and correlating with the severity of nonalcoholic fatty liver disease (NAFLD).[27] Targeting p16+ or senescent cells in the liver reduces steatosis, mitigates chemotherapy‐induced toxicity, and attenuates NAFLD progression in mice.[27, 28]. Here, CDKN2A is linked to steatosis.