The ability of HER3 to escape drug therapy, its resiliency and resourcefulness, and the multitude of feedback and crosstalk mechanisms that appear to come into play to ensure persistent tumour HER3 signalling activity despite the suppression of EGFR or HER2 by targeted therapies identifies HER3 as a focal point in HER family-induced transformation and a new biomarker and target for future cancer therapies. The gene discussed is EGFR; the disease is neoplasm.