Nevertheless, studies have proposed targeted interventions, including downregulating GOT2 via MYC/HIF-1α inhibition, developing allosteric inhibitors targeting the acetylation site K159 to induce tumor oxidative stress, and combining GOT2 inhibitor AOA with anti-GPC3 CAR-T therapy (such as BOXR1030) to enhance T-cell activity by depleting aspartate in the tumor microenvironment (36, 44, 58). The gene discussed is GOT2; the disease is neoplasm.