A simple genetic strategy involving loxP-flanked alleles encoding CPT2 (Cpt2fl/fl) has provided the means with which to disrupt FAO within specific mouse cell types6. This is potentially important, because much of the evidence indicating that FAO is required for fatty acid oxidation (FAO) 1–4. Mitochondriadependent β-oxidation of long-chain fatty acids requires the carnitine palmitoyltransferase (CPT) system, which consists of one transporter and two mitochondrial membrane enzymes: CPT1 and CPT2 (ref. 5). This system facilitates the transport of long-chain fatty acids into the mitochon-To the Editor: Recently, there has been considerable interest in the role of intracellular metabolism as a regulator of the fate and function of cells of the immune system1, 2. In macrophages, the classical M1 activation program has been noted to rely on glycolysis, while the M2 program seems to require the induction of