To study the oncogenic effects imposed by RICTOR, we established a RICTOR cell panel utilizing a SNP-array to detect RICTOR copy number variations (CNVs) across 57 NSCLC cell lines, and selected 7 RICTOR amplified and 5 RICTOR non-amplified lines spanning diverse secondary mutational backgrounds, including KRAS, EGFR and ALK gene alterations (Supplementary Figure 2 and Supplementary Table 1). The gene discussed is KRAS; the disease is non-small cell lung carcinoma.