Normalizing the intestinal bile acid profile can restore intestinal epithelial stem cell function46, and increase colonic RORγ+ Treg cell counts that ameliorate host susceptibility to colitis47, while LCA stimulates Treg differentiation and inhibits Th17 cells48 consistent with GUT-108’s ability to restore secondary bile acid metabolism (Fig. 4f) and activate inducible IL-10+ RORγ FoxP3+ CD4+ Treg cells (Fig. 3f). This evidence concerns the gene FOXP3 and Leber congenital amaurosis.