As shown by Nakagawa et al., WZ4002, a mutant EGFR-TKI, and E7050, a mutant selective dual inhibitor of Met and VEGFR-2, were able to inhibit tumor growth in Erlotinib resistant NSCLC cells in vitro and in vivo when given together with successful inhibition of the EGFR, Met, and their downstream PI3K-AKT pathway [79]. This evidence concerns the gene AKT1 and neoplasm.