Our data so far have proved that HOXA11-overexpressed GC cells upregulate the expression of Egr1 in HMrSV5 cells through forming a PDGF BB/TGF β1-miR-181a-5p feedforward loop with mesothelial cells, and prior studies found that Egr1 knockdown lessened liver fibrosis in a mouse model of thioacetamide-induced liver injury [26], moreover, Egr1 could favor alcohol induced steatosis [27] and human fibrotic disorders [9], however, there was no study focusing on the mechanism underlying Egr1 mediates mesothelial fibrosis and the effect of Egr1-overexpressed mesothelial cells on GC cells. This evidence concerns the gene EGR1 and steatosis.