Naïve BM ILC2s show high RANKL expression up-regulated by IL-2, IL-7, and all-trans retinoic acid, while BM ILC2s activated by IL-33 suppress RANKL expression and induce the differentiation of progenitors; BM-derived monocyte/macrophage lineage cells (BMMs), into M2 macrophage via abundant IL-13 and GM-CSF production.[14] Andreev et al reported that the ILC2s- IL-5 axis stimulated by IL-33 and IL-25 induced the production of a specific subtype of eosinophils, regulatory eosinophils (rEOS), in the joint that stimulated arthritis resolution. The gene discussed is IL5; the disease is arthritic joint disease.