The new insights into the relationship between IL-10 and lipid metabolism point towards novel targets for the treatment of inflammatory bowel disease and possibly beyond: Inhibition of CerS2 and targeting REL could limit ceramide production and exogenous addition of mono-unsaturated fatty acids might circumvent IL-10 deficiency and push macrophages towards an immunosuppressive and resolving phenotype. This evidence concerns the gene IL10 and inflammatory bowel disease.