Therefore, we assumed that EGFR promotes HER3 overexpression through the STAT3-mediated activation of G9a to repress the expression of HER3-targeted microRNAs, because we identified that STAT3, an EGFR downstream phosphorylated target, participates in tumorsphere formation and survival in EGFR-positive colorectal cancer cell lines [15]. This evidence concerns the gene STAT3 and colorectal cancer.