The significantly decreased CXCL1 expression in macrophages by eomdin treatment may be a key step to inhibit SAP-ALI, because macrophages can mediate and amplify the inflammatory cascade during the pathological progress of SAP by secreting CCL2, CXCL1, IL-1β, and other pro-inflammatory mediators (Shamoon et al., 2016; Jiménez-Alesanco et al., 2019). This evidence concerns the gene CXCL1 and acute respiratory distress syndrome.