We can conclude that in our model, the exposure to GWI-related chemicals and restraint stress resulted in a low-level inflammation of the liver which, after cholestasis challenge, caused an increased inflammatory reaction, with very high recruitment of CD11b/c+F/80−CD68− macrophages, enhanced proliferation of cholangiocytes, activation of HSCs, and ultimately increased liver fibrosis. Here, ITGAM is linked to cholestasis.