The HIF-1α-induced increase in glucose uptake is crucial for hypoxia-induced apoptosis resistance, suggesting that targeting HIF-1α and its effectors could be a novel therapeutic strategy for pediatric tumors.120 Moreover, HIF-1α hinders antigen presentation by downregulating MHC class I molecules and suppressing NKG2D ligands, helping tumor cells evade recognition by CD8+ T cells and NK cells.121,122 It recruits and expands MDSCs, which decrease T cell responses through several methods. The gene discussed is HIF1A; the disease is neoplasm.