Immune-based therapies have been developed to specifically reduce T2 immune cell activity either by blocking the pro-inflammatory cytokine loop (using, for example, anti-IL-5, IL-13, or IL-4, monoclonal antibodies) or by blocking activating-receptor fixation (using, for example, anti-IgE monoclonal antibody preventing IgE fixation to FcεRI, omalizumab®), significantly increasing various outcomes, including exacerbation rates, and improving pulmonary function tests in patients with T2-associated asthma not responding to inhaled corticosteroid treatment (ICS) (7). The gene discussed is IL5; the disease is asthma.