YAP is activated by stiffer substrates and translocated from the cytoplasm to the nucleus.20 The enhanced activation of YAP leads to malignant cancer phenotypes, such as metastasis,21 contact inhibition resistance,22 proliferation and epithelial-to-mesenchymal transition.23 Recent studies have suggested that the activity of YAP is inhibited by phosphorylation of the serine residue that occurs in a Hippo pathway-dependent or Hippo-independent process.20, 22 The epidermal growth factor receptor (EGFR) is a transmembrane tyrosine kinase that is overexpressed in roughly 40% of breast carcinomas. This evidence concerns the gene EGFR and cancer.