The activation of Th17 cells by IL-23 and Pam3CSK4, an agonist of TLR2/1, can lead to the increased expression of FASN, subsequently contributing to the survival and proliferation of Th17 cells; the inhibition of FASN, particularly in Th17 cells, significantly attenuated the disease in a mouse model of experimental autoimmune encephalomyelitis; Conversely, the inhibition of FASN function promotes the production of IFN-γ by Th1 and Th1-like Th17 cells [12]. This evidence concerns the gene FASN and experimental autoimmune encephalomyelitis.