UVB fails to upregulate sPmel17 and FHL2 in mouse hair follicles, so we assume that the activation mechanism of the sPmel17/FHL2/E-cadherin axis by UVB irradiation might play a role in the later stage of perifollicular repigmentation that occurred in patients with vitiligo, in which melanoblasts become mature melanocytes to release excessive amounts of sPmel17. Here, FHL2 is linked to vitiligo.