Despite the promising initial response of EGFR-mutant NSCLC patients towards first (reversible), second (irreversible), and third (EGFR mutant specific) generations of EGFR tyrosine kinase inhibitors (examples depicted in Figure 1), patients generally developed acquired resistance (by a secondary mutation or activation of alternative pathways within the cancer cells) which illustrates the need for improved treatment strategies in this subset of lung cancers [4,5]. The gene discussed is EGFR; the disease is cancer.