KRAS and neoplasm: As PDAC is driven by somatic rather than germline KRAS mutations and the tumor cellularity was ensured to be sufficient and comparable in all samples used in this study, we may hypothesize that the allele frequency may have at least some predictive value regarding the proportion of tumor cells carrying a mutation of the respective gene (i.e., percentage of tumor cell subclones with a pathogenic KRAS mutation) in this cohort.