DPP4 and neoplasm: HMGCL increases β-hydroxybutyric acid (β-OHB)-mediated acetylation of DPP4 at histone 3 lysine 9 (H3K9) and promotes its expression, leading to increased vulnerability of HCC cells to erastin- and sorafenib-induced ferroptosis.177 This observation suggests that HMGCL functions as a tumor suppressor by increasing ferroptosis susceptibility driven by β-OHB-mediated acetylation of DPP4.