Asthma is a complex respiratory disorder characterized by marked heterogeneity in individual patient disease triggers and response to therapy. Several asthma phenotypes have been identified, each defined by a unique interaction between genetic and environmental factors, including inflammatory, clinical and trigger-related characteristics. Different endotypes of asthma, based on the inflammatory pattern, may be regarded as T2-high (T2) or T2-low asthma, have led to the development of biological treatments targeting different inflammatory mediators. The hallmarks of T2 asthma are increased levels of blood and sputum eosinophils and other markers such as serum IgE, fractional exhaled nitric oxide and periostin. In clinical practice, omalizumab, an anti-IgE antibody biologic treatment, significantly reduced asthma exacerbations. Two different anti-IL-5 humanized monoclonal antibodies, mepolizumab, reslizumab and benralizumab as anti-IL-5Rα, significantly reduced the risk of exacerbations and improved lung function compared to placebo. Improving the understanding of T2-high and T2-low mechanisms and biomarkers may help to advance treatment options for many patients with asthma who remain uncontrolled despite the use of current standard of care.