However, tyrosine phosphorylation on the EGFR mutants could be further increased by EGF stimulation (Figure 2B), suggesting that the mutant EGFRs exhibit both ligand-independent and ligand-dependent activation, similar to that observed upon EGF stimulation of the L858R mutant H3255 lung adenocarcinoma cell line [21]. The gene discussed is EGF; the disease is lung adenocarcinoma.