Treatment of cancer with molecularly targeted agents that modulate specific genetic abnormalities like VEGF (vascular endothelial growth factor), EGFR (epidermal growth factor receptor), or BRAF has met with limited success because their specificity is too narrow: the built-in phenotypic plasticity or flexibility (20, 21) of the cancer epigenome facilitates rapid and recurrent compensatory adaptation, and the energetic costs that may constrain adaptation are evidently not prohibitively expensive. Here, EGFR is linked to cancer.