Considering that HER2 gene amplification generates highly redundant mRNAs that harbor multiple miRNA binding sites, we speculate that HER2 mRNA acts as ceRNA and can sequester endogenous miRNAs within HER2 positive breast cancer cells, thus cross-regulating the stability and translational efficiency of other host mRNAs with shared miRNA response elements. This evidence concerns the gene ERBB2 and breast cancer.