Our results showed CH12 inhibited the tumor growth of U251-EGFRvIII and U87-EGFRvIII xenografts in vivo and inhibited EGFR downstream signals, including the phosphorylation of AKT, ERK (partially) and STAT5, but had no effect on the critical mTOR pathway (Figure 1). This evidence concerns the gene STAT5B and neoplasm.