In conclusion, it was shown that overexpressing p130 or E2F4 increased the retention of mMSCs in the lungs of ARDS mice and promoted the differentiation of mMSCs into AT II, thereby improving lung permeability and pulmonary fibrosis, reducing pulmonary oedema and further contributing to an improved therapeutic effect of mMSCs on ARDS mice. The gene discussed is E2F4; the disease is pulmonary edema.