For example, in a KRASG12D PDAC mouse model treated with MRTX1133, KRAS inhibition resulted in deep tumor regression, ultimately leading to the emergence of resistance.204 These findings reflected the molecular amplification of KRAS, Yap1, Myc, Cdk6, and Abcb1a/b, as well as the coevolution of drug resistance transcriptional programs.204. This evidence concerns the gene KRAS and neoplasm.