We selected FAK for further analysis for the following two reasons: (i) our previous studies using phosphoproteomic profiling showed that miR-204 overexpression resulted in reduced expression/phosphorylation of FAK (and other kinases) which was associated with vasculogenic mimicry inhibition in two triple negative breast cancer cell lines [18,19] and (ii) FAK is a well-known protein involved in cell migration, which is essential for the development of channel structures during vasculogenic mimicry. The gene discussed is PTK2; the disease is triple-negative breast carcinoma.