Next, we confirmed that a high proportion of intestinal ckit+FcERI+ MC produced GM-CSF, to a similar extent as the Thy1+IL7R+ ILC (Fig. 5d) that were described recently as a major source of GM-CSF in our study of colitis31 and in the joints in a model of rheumatoid arthritis (RA)36. This evidence concerns the gene CSF2 and rheumatoid arthritis.