The non‐receptor tyrosine kinase c‐Src was involved in STAT3 activation in many types of cancer cells.[29] To validate whether co‐transfection of c‐Src would enhance STAT3 MVEs translocation bedsides the reported nuclear translocation, STAT3‐R31K and STAT3‐C108G mutants were co‐transfected with c‐Src, and autonomic MVEs translocation emerged without LIF stimulation (Figure 2I). This evidence concerns the gene STAT3 and cancer.