To validate the effect of SREBP-2 inhibition as a therapeutic target on infectious diseases with septic shock, we utilized the cecal ligation and puncture (CLP) model for recapitulating pathophysiology of sepsis.39 The exogenous incorporation of Fatostatin A and SN50 recovered the mRNA levels of Srebp2, Sens1, and Pcsk9 to lower range (Supplementary Fig. 5a–c). The gene discussed is SREBF2; the disease is Sepsis.