The increased expression of Shh in injured lung tissue activated the Shh signaling pathway and its downstream key target protein Wnt3a during BMSC engraftment into the lung, thereby driving the differentiation of BMSCs into AT2 cells and ultimately promoting AT2 cell regeneration to repair injured alveolar epithelium and subsequently improve lung function in LPS-induced ALI/ARDS. The gene discussed is WNT3A; the disease is acute respiratory distress syndrome.