As we know that frequent STAT3 activation in cancer cells is largely due to the fact that STAT3 is a point of convergence for numerous tyrosine kinases, including PDGFR, EGFR, AKT, SRC and JAK family, etc. [37] However, eEF2K depletion did not affect the activity of these proteins, suggesting eEF2K may regulate the activity of STAT3 via a previously uncharacterized mechanism. The gene discussed is SRC; the disease is cancer.