METTL3 and pulmonary fibrosis: For example, genetic and pharmacological inhibition of METTL3 alleviated renal inflammation and injury both in vitro and in vivo.[29] METTL3‐mediated m6A modification was found to play a profibrotic role in the postinfarct myocardium, and silencing METTL3 mitigated collagen production both in vitro and in vivo.[30] Notably, an intervention targeting METTL3‐mediated m6A modification inhibited the fibroblast‐to‐myofibroblast transition (FMT) in pulmonary fibrosis.[16] Here, we revealed a novel role of m6A modification in regulating RILI.