In a follow-up study using LSL-KrasG12DRosa26-LSL-MycERT2 transgenic mice, with constitutive expression of KrasG12D and inducible expression of MycERT2, it was proposed that, while the KrasG12D mutation alone was sufficient to induce preneoplastic lesions, the additional activation of Myc led to rapid acceleration of tumourigenesis, hence transforming indolent tumours to adenocarcinomas [30]. Here, MYC is linked to neoplasm.