MARK1 and fibrosis: These might be resulted from that (a) miR‐125b promoted inflammatory cells and mediators via regulating inflammatory signaling pathways such as p38 MARK/NFκB pathway, thus sepsis patients who were featured as severe inflammation presented with increased level of miR‐125b14; (b) miR‐125b would induce several organ dysfunctions or failures such as promoting cardiac fibrosis and fibroblast‐to‐myofibroblast transition, and acute‐on‐chronic liver failure, thus sepsis patients who were characterized as multi‐organ dysfunction or failure presented with increased level of miR‐125b.15, 16