We have elucidated a dual mechanistic paradigm wherein: in HPV18+ AC and HPV− SCC, hypoxia-mediated HIF-1α activation suppresses ATXN3 expression, leading to decreased P53 stability and consequent tumor progression; while in HPV16+ SCC, hypoxia-induced HIF-1α upregulates ATXN3 expression, which drives oncogenesis through STAT5 phosphorylation—likely mediated through stabilization of its upstream kinase p-JAK3. The gene discussed is HIF1A; the disease is neoplasm.