Researchers have found that there is an increased level of aerobic glycolysis and lactate production in fibrotic lung tissue [10, 11, 20], and our previous research also demonstrated that LPS could induce lung fibroblast aerobic glycolysis and lactate production through PI3K-Akt-mTOR/PFKFB3 pathway activation, thus promoting collagen synthesis and pulmonary fibrosis [13]. The gene discussed is PFKFB3; the disease is pulmonary fibrosis.