Given that the pathophysiology of CRSwNP is primarily driven by eosinophilic inflammation, involving T-helper cell 2 cytokines and IgE production [29], biological therapies with monoclonal antibodies—originally developed for conditions like asthma or atopic dermatitis, which share an underlying type 2 inflammatory pathway—can also be utilized for type 2 CRSwNP. The gene discussed is IGHE; the disease is atopic eczema.