They proposed a possible model for the genomic evolution of pancreatic cancer as being a consequence of a gene expression continuum from (a) both Basal-like and Classical cell populations, and (b) linked to allelic imbalances in mutant (mt) KRAS, with metastatic tumors being more copy number-unstable compared to primary tumors (Chan-Seng-Yue et al., 2020). This evidence concerns the gene KRAS and pancreatic neoplasm.