In viral pneumonia, PI3K/Akt activation also participates in inflammatory regulation: on one hand, it promotes NF-κB activation by phosphorylating IκB, inducing the production of inflammatory factors such as IL-6 and TNF-α, which can easily trigger cytokine storms and ARDS; on the other hand, this pathway participates in the M1/M2 phenotype conversion of macrophages and the regulation of the TLR/mTOR axis, affecting immune metabolic reprogramming and tissue repair in the lungs (Zhao et al., 2014). This evidence concerns the gene TNF and acute respiratory distress syndrome.