This pathway is believed to be able to moderate the Th1/Th2/Th17 imbalance in psoriasis.215 After being activated by cytokines, mTOR is also involved in the secretion of proinflammatory molecules, such as CXCL8, IL-6, and VEGF, by keratinocytes.226 It has been suggested that mTORC2 might be essential for FOXP3 stability mediated by chemokine CCL3.227 Notably, overactivated mTORC1 contributes to parakeratosis (nuclei retention), which is a form of pathological change of psoriasis.228 In brief, the mTOR axis serves as a crucial regulator of inflammation and cell proliferation in psoriasis. Here, FOXP3 is linked to psoriasis.