Studies have shown that the upregulation of the PI3K-AKT signaling pathway leads to mTOR activation and exacerbates bleomycin-induced pulmonary fibrosis when lung epithelial cell autophagy levels fail to inhibit apoptosis.[29] In addition, AKT inhibitors effectively inhibit fibroblast differentiation in lung tissue and reduce collagen I and III levels.[36] This finding suggests that YTG may achieve antifibrotic effects through combined signaling pathway inhibition. Here, AKT1 is linked to pulmonary fibrosis.