Previous studies proved that IL-6 can activate the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway, induce an inflammatory response, and possibly form a cytokine storm, which is an important factor for the development of ARDS and extrapulmonary organ damage, and that an IL-6 receptor antagonist can suppress the over-activation of the human immune system [7]. Here, IL6 is linked to acute respiratory distress syndrome.