Abstract: Cutaneous T-cell lymphoma (CTCL) represents a heterogeneous group of non-Hodgkin lymphomas that originate in the skin, and are often challenging to manage at advanced stages. In recent years, the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway has garnered significant attention due to its established roles in the pathogenesis of various inflammatory diseases and tumors. However, whether the JAK/STAT pathway can serve as a therapeutic target for CTCL remains inconclusive. Notably, some clinical reports have suggested that JAK inhibitors may potentially increase the risk of CTCL onset. This review summarizes current clinical research progress regarding the role of the JAK/STAT pathway in the development and progression of CTCL, as well as the dual potential of JAK inhibitors to either treat or trigger the disease.