KRAS and neoplasm: used an amplicon-based NGS strategy with UMIs to assess two KRAS codons (G12 and Q61) in ccfDNA from 221 patients with stage I-II PDAC.[5] They found that 30% of patients had somatic tumor mutations detectable in ccfDNA with a median VAF of 0.12% (range: 0.01 to 1.31%) [5], which is similar to our reported findings in a stage II-III PDAC cohort that found ctDNA associated with 4 genes on our 118 gene panel.