Consequently, in the hypoxic OSA microenvironment, STAT3-mediated signaling may cooperate with HIF1α to maintain high levels of xCT and potentially amplify CSPG4 and TLR2 expression, linking TP53/RB1 deficiency to invasive, stress-resistant, and immunomodulatory tumor phenotypes. The gene discussed is HIF1A; the disease is neoplasm.