Pro-inflammatory macrophages (Mø) are crucial for onset of intestinal inflammation, and defects that enable persistence of these cells may contribute to inflammatory bowel disease. We recently showed that the ErbB4 receptor tyrosine kinase is induced on Mø by pro-inflammatory activation, and that subsequent stimulation with the ErbB4-specific ligand neuregulin-4 kills these cells. This suggests that Mø-expressed ErbB4 limits inflammation, but the cell type specificity of this effect and the role of ErbB4 in regulating colitis onset and recovery in vivo is untested.