Thus, some degree of overexpression of a mutant form of p110α that cannot bind to RAS is enough to suppress the activation of the PI3K-AKT pathway in several EGFR-oncogene-driven lung cancer cell lines, including those with additional EGFR T790M resistance mutations and also MET amplification, providing evidence of dominant-negative activity of the RBD-mutant p110α protein over the WT form of the protein. This evidence concerns the gene EGFR and lung carcinoma.