However, a report by a different research group shows that mice lacking cFLIP in CD11c-expressing cells were found to develop neutrophilia (caused by excessive production of granulocyte colony-stimulating factor receptor, (G-CSF)) and splenomegaly, but do not spontaneously develop arthritis, potentially owing to either differences in the efficiency of cFLIP deletion or variability in colony environment [67–70]. The gene discussed is CSF3; the disease is arthritic joint disease.