Although Chr-A has been proven to attenuate proliferation, induce DNA damage, promote apoptosis and cause cell cycle arrest, inhibiting the progression of various tumors, such as leukemia [61], KRAS-mutant lung adenocarcinoma [27] and glioblastoma [28,29], the antitumor effects of Chr-A in a glioma orthotopic model and whether Chr-A regulates metabolism reprogramming were previously unclear. The gene discussed is HRAS; the disease is leukemia.