Finally, epigenomic profiling via CUT&Tag reveals differential H3K4me3 enrichment at key inflammatory and myeloid differentiation loci, including Tlr4 and E2F targets, which may contribute to the heightened inflammatory responsiveness of HSPCs for nonresolving myelopoiesis in HFD-induced obesity. The gene discussed is TLR4; the disease is obesity due to melanocortin 4 receptor deficiency.