HIV-1 Tat interactive protein 2 (HTATIP2) is also a tumor suppressor; by enhancing the HIF2α-regulated β-catenin/c-Myc/MCL-1 signaling, HTATIP2's deletion increases tumor metabolic plasticity, that is, enable tumor cells to exploit alternative metabolic pathways for replenishing TCA cycle intermediates, to avoid dependence on carbon sources from glutamine and fatty acid, thus inducing LUAD cell survival and proliferation [36]. This evidence concerns the gene MYC and neoplasm.