Increasing evidence supports a potential role of STAT3 as a tumor driver in CTCL [3,5,9,10,15,16,17,18,19], and most human SS cells and CTCL cell lines display constitutively activate phosphorylated STAT3 (p-STAT3) with STAT3 inhibition resulting in massive apoptosis [20,21,22]. The gene discussed is STAT3; the disease is neoplasm.