Based on the aggressive TNBC tumor biology and high proliferation indices of most TNBC, we hypothesize that EGFR-driven TNBC tumors are uniquely suited for a SIAH-centered biomarker discovery program as well as development of anti-SIAH-based targeted therapy by targeting this conserved and essential signaling bottle neck, SIAH, to shut down this highly adaptive EGFR/RAS/RAF/MEK/MARK signaling network that drives chemo-resistant, relapsed, and metastatic TNBC in the clinic (Figure 1). The gene discussed is MAP2K7; the disease is neoplasm.