CCDC88B and colitis: The reason for this seemingly contradictory result can only be speculated on at the moment, but could involve different mutation-specific effects on cellular responses at the site of inflammation, with cellular infiltrates of different leukocytes composition including strong granulocytes content in Arhgef2 vs. Ccdc88b. The compensatory granulocytic response during colitis in Arhgef2−/− mice is similar to other mouse mutants with DC-deficiency, including Irf1 mutants27.