Most importantly, in addition to phosphorylation of Erk canonical targets, MEDICA-activated Erk resulted in serine/threonine phosphorylation of Erk downstream receptor tyrosine kinases (RTKs) and transduction elements that serve as oncogenic drivers of resistant B-Raf(V600E) cancers, including EGFR(Thr669), STAT3(Ser727), FAK(Ser910) and IRS1(Ser636/639), while suppressing basal phospho-Akt(Ser473) (Figure 4B). Here, BRAF is linked to cancer.