However, tocilizumab was able to more strongly reverse a handful of relevant ARDS effectors: 1) obviously, pleiotropic interleukin IL-6 signalling and activity, involved in the cytokine storm induction; 2) BTK, a central signalling molecule in several immune-related processes; and 3) several effectors involved in epithelial and endothelial biology that have been related to epithelial damage and fibrosis, including cytokines (IL-4, IL-10, TGFA, VEGFA), proteins that regulate endothelial function (ACE2, AGT1R, ANGPT2, CDH5, EGFR, FN1, PTPRB, VEGFA) and involved in apoptosis (FASL, TRAIL). This evidence concerns the gene FN1 and acute respiratory distress syndrome.