EGFR and neoplasm: When EGFR is the genomic ‘driver’ of a tumor (ie. EGFR mutation or EGFR amplification; inappropriately ‘pushing the gas pedal’), using targeted inhibition towards that driver generally has resulted in significantly improved clinical outcomes in that patient subset, (Petty et al., 2014; Zhang et al., 2013; Zhou et al., 2011) albeit until development of resistance with consequent progression (Figure 1C).