Previously, we demonstrated that enhanced HIF-1α expression in NP tissues may cause tissue neutrophilia and poor steroid response, and provided an alternative to restore steroid sensitivity by adding clarithromycin [13], and Wang et al. showed that the IL-36γ/IL-36R pathway play a critical role in the development of neutrophilic inflammation and corticosteroid resistance in CRSwNP patients [14]. The gene discussed is HIF1A; the disease is chronic rhinosinusitis with nasal polyps.