Demyelination is a hallmark of the peripheral nerve injury and is associated with the neurological dysfunction after peripheral damage. Because remyelination is required for recovery from neurological dysfunction, the mechanism of peripheral remyelination is thought to contribute to restoration of neurological function. We previously reported that the central nervous system remyelination was promoted when the brain was exposed by the circulating molecules, such as FGF21. Because the receptor for FGF21 is not limited in the brain, we asked whether FGF21 also regulated remyelination in the peripheral nervous system. To test this, we first investigated FGF21 receptor expression in mouse schwann cells. We detected beta-klotho, which is a co-receptor for FGF receptors, in mice S100-positive cells in vivo and in vitro (cell line), suggesting that schwann cell can response to FGF21. Schwann cell proliferation is a process of schwann cell development, therefore, we evaluated whether FGF21 regulate schwann cell proliferation. By bromodeoxyuridine (BrdU) incorporation analysis, we found that FGF21 treatment prevented proliferation of schwann cells. These data provide the possibility that FGF21 is also involved remyelination in the peripheral nervous system.