Notably, the use of the gut-corrected Tg(FABP-hCFTR) CF mouse to propose Cftr-dependent regulation of phagosomal acidification as a key mechanism behind defective intracellular bacterial killing in CF macrophages was a major finding in the field, but spawned much controversy and has ultimately not proven reproducible despite the use of more accurate ratiometric methods with greater pH sensitivity than the fluorescein-based techniques employed in the original study [26], [27], [28]. This evidence concerns the gene CFTR and cystic fibrosis.