Our preliminary studies illustrated that LPSs could activate the phosphoinositide3-kinase-Akt (PI3K-Akt) pathway via TLR4 in primary cultured mouse lung fibroblasts, which subsequently promoted the synthesis of α-SMA and the activation of fibroblasts, thereby directly promoting collagen secretion and accelerating the process of pulmonary fibrosis through the upregulation of integrin β1 expression[8]. The gene discussed is TLR4; the disease is pulmonary fibrosis.