In adult mice, recent data show that high-fat-diet-induced obesity triggered persistent epigenetic reprogramming in myeloid progenitor cells through stearic acid-induced Il1b expression.26 Likewise, in adult mice, exposure to IL-1bβ or β-glucan triggered trained immunity and increased glycolysis via HSPCs.15,69 Using an in silico analysis of RNA-seq and ATAC-seq from juvenile mWSD BMDMs, we found that IL-1B could be an important upstream regulator. The gene discussed is IL1B; the disease is obesity due to melanocortin 4 receptor deficiency.