Previous studies have shown that cancer cells under stressful conditions, such as hypoxia, can adapt metabolically by increasing acetate utilization via ACSS2 to support proliferation and survival.43 The healthy mucosa of the large intestine is already under physiological hypoxic conditions and, as the tumors form and grow, the hypoxic environment is only further exacerbated.44,45 Therefore, increased ACSS2 expression in KRAS G12V cells and their inherent increased utilization of acetate may favor KRAS G12V adenoma formation and continuous growth in a hypoxic colorectal environment. Here, KRAS is linked to adenoma.