The above results suggest that further overexpression of HIF-1a partially reverses the hindering effect of sh-XBP1 on the development of CRSsNP in mice by exacerbating pathological changes in mouse nasal mucosal tissues, promoting inflammation, and activating the Wnt/β-catenin pathway. The gene discussed is XBP1; the disease is chronic rhinosinusitis without nasal polyps.