The etiology of resistance to ERBB2-directed therapies has been widely investigated in breast cancer [7]–[15]; the accepted resistance mechanisms included constitutive activation of the PI3-K pathway [7], [9], truncated p95 isoform of HER2 receptor which cannot bind to trastuzumab [15], and constitutive Src activation as a common node downstream of multiple pathways [10]. Here, SRC is linked to breast cancer.