In addition, while TMEM16A antagonism or deficiency was found earlier to ameliorate bronchial hyperresponsiveness in the Ova mouse model of allergic asthma (Zhang et al., 2013; Wang et al., 2018) that is dependent on eosinophils and Th2 inflammation, it remains unexplored in newer models of asthma exacerbations and COPD that are steroid-resistant (Ito et al., 2008; Fricker et al., 2014; Jones et al., 2017) in which neutrophils and/or macrophages serve a greater role. The gene discussed is ANO1; the disease is allergic asthma.