Finally, across GU-1 and GU-2, WES analysis of CTCs identified high AF variants within known cancer genes, beyond those detectable using ctDNA or even tissue needle biopsies, including premature stop codons in ASLX2, IL6ST, and SIN3A genes, and potential pathogenic missense mutations in genes involved in homologous recombination, cell cycle checkpoints and chromatin regulation (ATM, BRCA1, BRCA2, CHD2, CHD4, CHEK2, FANCA) (Fig. 6B, C). This evidence concerns the gene CHD4 and atrial fibrillation.