Based on the knowledge that i) TLR4 is required and sufficient for the hyperketonemia-normalizing action of S100A9 (Fig. 1E, F), ii) TLR4 activates the mTOR axis downstream of the TRIF/TRAM pathway41,47,48, and iii) mTORC1 suppresses fasting-induced hyperketonemia10, we investigated whether mTORC1 is a key molecular component of the pathway(s) underling the hyperketonemia-normalizing action of S100A9 in diabetes. The gene discussed is MTOR; the disease is diabetes mellitus.