Altogether, our study indicates that the miR-124/STAT3 axis plays a relevant mechanism in CTCL pathogenesis thorough the regulation of a whole transcriptional signature particularly involving the MYC pathway, which is an essential tumor driver in multiple systems, among other factors (Syndecan, TFAP2C, RPTOR DOK-1, IL-7, IFI35, CXCL9, or BCR) that may constitute potential therapeutic targets in CTCL. This evidence concerns the gene IFI35 and neoplasm.