However, treatment with TUDCA, which is known to reduce experimental colitis by abolishing ER stress in colonocytes [41], partially rescued the vitamin D3-induced depletion of LGR5-GFP-positive cells and reduced the number of cleaved caspase-3-positive cells in intestinal organoids, suggesting that the depletion of stemness and apoptotic cell death induction by vitamin D3 may be mediated by ER stress induction. The gene discussed is CASP3; the disease is colitis.