At the end of the experiment, tumors from WT-p110α or parental PC9 cells were 10-fold larger than tumors from PC9 MUT-p110α cells (Figure S2A), while in H1975 cells, the differential was 10,000-fold (Figures S2B and S2C), demonstrating that expressing an RBD-mutant form of p110α that cannot bind to RAS abrogates the growth of EGFR-driven human NSCLC cell lines in vivo in a tumor cell-autonomous manner. The gene discussed is EGFR; the disease is non-small cell lung carcinoma.