The TP53R273H−BCAR1 complex may induce gene expression only when SFKs are activated by upstream signals triggered by either binding between the extracellular matrix and integrin receptors or binding between growth factors and cell-surface receptors such as receptor tyrosine kinases.37 The development of drugs that block BCAR1 phosphorylation and translocation into the nucleus, interfere with the TP53R273H−BCAR1 interaction, or degrade TP53R273H, could be effective strategies to inhibit the TP53R273H−BCAR1-mediated invasion in cancer. Here, CD177 is linked to cancer.