KRAS and neoplasm: Based on the clonal/subclonal mutation information, a parsimonious evolutionary history for P042 can be proposed: first, clonal driver mutations (TP53 and KRAS mutations) appeared early in the primary site (i.e. tumor initiation) followed by subsequent genetic alterations (concurrently or separately) that formed a number of subclones (tumor progression); then a single cell from a minor subclone that acquired an invasive phenotype (marked by mutations such as MUC16:M9930I), migrated to a distant organ (liver in this case) and successfully established a metastasis.