ANO1 and allergic asthma: While these initial studies solidified TMEM16A’s role in the bronchial epithelium as responsible for the elevated Ca2+-dependent chloride secretion induced by Th2 cytokines, subsequent studies by Huang et al. (2012) expanded this perspective suggesting TMEM16A may have a dual role in controlling both ASM contraction and epithelial mucin secretion, a hallmark of allergic asthma.