Other mechanisms of NF-κB activation in CLL that have recently come into the limelight include an unexpected role for BTK, which has been found to directly interact with and to phosphorylate IκBα, which does not undergo degradation [133], and the engagement of the microenvironmental factor Wnt5a with Receptor tyrosine kinase-like Orphan Receptor 1 (ROR1), an oncoembryonic orphan receptor, resulting in an autocrine signaling loop triggered by Signal Transducer And Activator Of Transcription 3 (STAT3) via NF-kB-mediated expression of IL-6 [134]. This evidence concerns the gene STAT3 and B-cell chronic lymphocytic leukemia.