We hypothesized that abundances of pro-inflammatory microbiota, including E. coli, would differ in CF fecal samples from participants with high versus low levels of fecal inflammation, and that restoration of CFTR function with ETI would reduce fecal abundances of pro-inflammatory pathogens in parallel with fecal calprotectin relative to pre-treatment. This evidence concerns the gene CFTR and cystic fibrosis.