The first report on afatinib in cellular models of lung cancer initially assessed the effects in two mechanism-based models exclusively driven by oncogenic EGFR mutations, namely, anchorage-independent proliferation of NIH-3 T3 murine fibroblast cells expressing mutant EGFR and IL-3 independent proliferation of the Ba/F3 murine pro-B cell line (Li et al. 2008). The gene discussed is EGFR; the disease is lung cancer.