When accumulated in colorectal cancer (CRC) cells at >100 μM (a concentration driven by Warburg effect-impaired butyrate oxidation), it functions as a potent HDAC inhibitor: this activity suppresses cell proliferation, induces apoptosis, and drives downstream effects like Pyruvate Kinase M2 activation (47) and reactive oxygen species (ROS)-induced apoptosis (48), resolving its paradox by prioritizing tumor suppression in malignant cells. The gene discussed is HDAC9; the disease is neoplasm.