In the case of CFTR involvement in phagolysosome acidification and ensuing intracellular killing of pathogens by phagocytes, it is worth mentioning that this is a controversial issue, since opposite results were obtained, i.e., a non-CFTR pathway to acidification or even a lack of acidification in CF monocytes/macrophages [36,37,38], demonstrating how different models and investigation techniques may compound the already intrinsic patient-to-patient variability. The gene discussed is CFTR; the disease is cystic fibrosis.