(2013) selected and transplanted the resistant tumor clones into Severe Combined Immunodeficient (SCID) mice and resumed the Selumetinib treatment and showed that the resistance of BT-40 xenografts to Selumetinib was mediated by activation of STAT3 signaling, so STAT3 activation could be compensating for MEK inhibition to maintain proliferation and survival (50). The gene discussed is STAT3; the disease is neoplasm.