Regarding fatty acid oxidation, our data show that infection promoted the upregulation of Acot1, Acot2 and Acot8, which encode acyl-CoA thioesterases, a group of enzymes that hydrolyze acyl-CoA esters into free fatty acids and coenzyme A. These enzymes balance the capacity of fatty acid oxidation, triglyceride levels and mitochondrial function (Franklin et al. 2017; Moffat et al. 2014). Here, ACOT2 is linked to infection.