In breast cancer cells, transmembrane CD44 isoforms have been shown to either physically associate directly with JAK2 and STAT3 to induce conventional STAT3 oncogenic signaling (80) or activate STAT3 in the cytoplasm to form a complex with NF-kB p65 subunit in order to initiate the transcription of human telomerase reverse transcriptase (hTERT), which further leads to EMT and breast CSC phenotype maintenance (81). This evidence concerns the gene NFKB1 and breast cancer.