In particular, because type 2 inflammation is a frequent hallmark of severe asthma and CRSwNP, comorbid patients can significantly benefit from treatments targeting pathophysiologic pathways operated by several effector molecules including IgE, IL-5, and its receptor, as well as the receptors of IL-4 and IL-13 (Figure 1) [89]. The gene discussed is IL5; the disease is chronic rhinosinusitis with nasal polyps.