In preclinical models of inflammatory disease, we have previously demonstrated the critical role of eNAMPT-induced TLR4 signaling in determining the severity of several inflammatory disorders (ARDS, radiation lung injury, pulmonary hypertension, and lupus vasculitis), utilizing the humanized eNAMPT-neutralizing mAb, ALT-100.14,18,21,24,25 The therapeutic efficacy of ALT-100 mAb (0.4 mg/kg, once per week IP) was assessed in the STZ/HFD NAFLD model with ALT-100 mAb delivery beginning at week 9 and continued weekly through week 12. This evidence concerns the gene TLR4 and pulmonary hypertension.