Figure 6A details the interplay between STAT3 and RhoC in this setting. It has been shown that elevated RhoC expression in HNSCC drives increased IL-6 production by a currently unknown mechanism, postulated to involve NF-κB and the Rho effector, Rhotekin. The expressed IL-6 functions in autocrine activation of STAT3 via IL-6R/JAK. Activation of STAT3 results in the transcription of stem cell transcription factors required for the tumourigenic nature of CSCs [53]. This evidence concerns the gene STAT3 and head and neck squamous cell carcinoma.