Moreover, BM-MSCs inhibited the inflammatory and phenotypic transformation of alveolar macrophages, thereby affecting the inflammatory phenotype of lung organoids through the NF-κB pathway.182 In the paraquat-induced ALI model, combined mitigation of the NF-κB and IL-17 signaling pathways in BM-MSC-transplanted samples was observed.183 The downregulation of MyD88-NF-κB signaling protein expression was also demonstrated in human UC-MSC treatment.184 Furthermore, research has indicated that BM-MSCs reduce the influx of CD8+ T cells within the intestinal region. The gene discussed is NFKB1; the disease is acute respiratory distress syndrome.