However, we found a constitutive activation of ERK in all PC9 GR clones, indicating that the cellular genetic background significantly contributes to the activation of different EGFR downstream effectors in EGFR-TKI-resistant cells, despite our results confirming that the AKT and/or ERK signaling pathways are also persistently activated when tumor cells are exposed to suboptimal doses of gefitinib, similarly to cells exposed to higher escalating doses of the drug [7,8]. The gene discussed is AKT1; the disease is neoplasm.