Since cytosolic FAK acts upstream of BRAF/NRAS, and nuclear FAK interferes with the activation of wtp53 as being expressed in the majority of melanomas, we investigated whether FAK inhibition may have an implication in current clinical applications, i.e. re-sensitizing MM cells that have overcome mutation-specific targeted kinase inhibition to cell death. This evidence concerns the gene PTK2 and Miyoshi myopathy.