Based on our data, we suggest that it may also be possible to manipulate the balance of the FER-PKCδ-PTPN14 axis to simultaneously inhibit downstream signals emanating from multiple RTKs to resensitize TNBC or other cancers that have developed adaptive resistance to MEK-I, ALK-I, or BRAF-I through up-regulation of multiple RTKs, without the need to determine which, and how many, RTKs are hyperactivated. The gene discussed is PTPN14; the disease is cancer.