Over 3 decades of CF research has demonstrated that lack of CFTR-mediated HCO3− secretion and subsequent ASL acidosis provides a convincing mechanism that leads to abnormal mucus and bacterial eradication (Stoltz et al., 2015) at least in the CF airways of neonates (Abou Alaiwa et al., 2014a; Abou Alaiwa et al., 2018). The gene discussed is CFTR; the disease is cystic fibrosis.