Longmin et al. showed that myeloid Kdm2a-/- mice were protected from HFD-induced injury (including obesity, insulin resistance, hepatic steatosis, and reduced macrophage accumulation in adipose), the underlying mechanism attributed to increased H3K36me2 levels of Pparg and subsequently M2 polarization by Kdm2a knockout 18. The gene discussed is PPARG; the disease is fatty liver disease.