This would be deleterious in conditions that favor thrombogenesis, such as within the cardiac left atrial appendage, the nidus for thrombus formation in AF that leads to CES.26Drugs in development aimed at inhibiting GPVI-dimer in stroke are demonstrating promising results.27It could be hypothesized that molecules such as glenzocimab, a humanized fragment of antibody (Fab) against platelet GPVI, which is able to cause thrombus disaggregation by interrupting GPVI–fibrin interactions,11may have a role to play in downregulating some of the GPVI–fibrin interactions in AF patients. This evidence concerns the gene GP6 and stroke disorder.