In previous clinical reports, gefitinib was effective in a few patients without EGFR mutations, thus indicating that not only mutations in TK domain but other mechanisms such as amplification, aberrant signaling may activate AKT and sensitise tumour cells to EGFR inhibitors (Amann et al, 2005; Takano et al, 2005). The gene discussed is EGFR; the disease is neoplasm.