While we and others have found that STAT3 activation confers high PD-1 and/or PD-L1 expression in CTCL tumor cells and other NK/T cell malignancies that may promote tumor immune evasion (43), our data specifically demonstrated that JAK/STAT and NF-κB pathways are major mediators of PD-1 expression in M2-like TAMs in CTCL. This evidence concerns the gene SOAT1 and neoplasm.