Activation of the mechanistic target of rapamycin (mTOR) signaling pathway may facilitate the translocation of HIF-1α from the cytoplasm to the nucleus, thereby increasing VEGF expression—a process that promotes angiogenesis while increasing vascular permeability, leading to pulmonary edema and damage to the pulmonary capillary endothelium, and an increase in inflammatory factor infiltration [93]. This evidence concerns the gene MTOR and edema.