Third, although we have confirmed that β-OHB inhibited LPS-induced mouse sepsis and the STAT1-K679R mutation weakened the anti-inflammatory effects of β-OHB in vivo (Fig. 10A–E), further research focus on constructing conditional myeloid cell-specific point mutation mouse (STAT1 p.K679R Lyz2-cre) to elucidate the significance of Kbhb modifications in the treatment of relevant inflammatory diseases, such as septic liver injury or obesity, is needed. The gene discussed is STAT1; the disease is Obesity.