The release of inflammatory factors, such as TNF‐α, could promote cell apoptosis, microvascular dysfunction, and tissue necrosis.37 The cumulative message of several recent studies has revealed that lncRNAs are abnormally involved in inflammation response and serve as effective therapeutic targets for pneumonia.32, 35 We put forward biological functions and mechanisms of XIST in pneumonia and firstly found that XIST knockdown lead to the inhibition of cell apoptosis and inflammation injuries in LPS‐induced WI‐38 cells by sponging miR‐370‐3p. The gene discussed is TNF; the disease is susceptibility to pneumonia measurement.