Zhang et al. discovered that the expression of AKT and p-AKT protein were significantly increased in lung tissue of IPF rats induced by bleomycin, while hirudin could obviously alleviate these abnormal expressions and slow down the progression of IPF, which illustrated that hirudin was likely to act on IPF through the PI3K/AKT pathway (Zhang et al., 2019). The gene discussed is AKT1; the disease is idiopathic pulmonary fibrosis.