A combination of soluble mediators, including GM-CSF, IL-17A, and TGF-β1 induced SAMac differentiation from circulating monocytes in vitro, while in vivo blockade of these mediators in the mouse carbon tetrachloride (CCl4) CLD model attenuated SAMac differentiation (102). This evidence concerns the gene TGFB1 and congenital secretory chloride diarrhea 1.