However, we did not observe this effect in RA MØIFN-γ. This might be due to the IFN-γ-induced M1-like phenotype, which could be modulated to a less inflammatory phenotype by Sema3B, but without reaching pro-resolving characteristics, as it would be the case for Sema3B-modulated RA MØM-CSF. The gene discussed is IFNG; the disease is rheumatoid arthritis.