SRC and neoplasm: These signaling interactions between growth factor receptors (the epidermal growth factor receptor (EGFR), hepatocyte growth factor receptor (c-Met), platelet derived growth factor receptor (PDGFR), vascular endothelial growth factor receptor (VEGFR), etc.)and cytoplasmic non-receptor tyrosine kinases and transcription factors (c-Src, c-Abl, JAKs, STAT3, β-catenin, etc.)not only synergize to promote tumor growth, survival, and metastasis, but also mediate resistance to targeted therapies through the activation of compensatory signaling pathways [1,2,3].