The inhibition of the interleukins IL-4 and IL-13 involved in the inflammatory process has, therefore, proved to be an effective therapeutic strategy to keep the three phenotypes of severe asthma under control, as well as the related type 2 pathologies, which often manifest as comorbidities in the patient with severe asthma, aggravating the clinical course [13]. The gene discussed is IL4; the disease is asthma.