However, the other three Type 2 cases with no directly observed tumor cells with normal Pten/chr19 exhibited a distinct pattern of cancer driver alterations, characterized by amplification of oncogenes, including Hras, Ccnd1, and c-Myc in Mouse 5 tumors; Fgfr2, Olig2, Foxo1, and Cdk4 in Mouse 10 tumors; and Met, Ret, Ccnd2, and N-Myc in Mouse 4 tumors (Fig. 6i–k). This evidence concerns the gene HRAS and neoplasm.