Thus, CLEC-2 and GPVI could be particularly interesting, with a possible advantage for CLEC-2, as demonstrated in murine models of sepsis (LPS injection or cæcal ligation puncture) where the platelet CLEC-2 receptor is knocked out or inhibited by a monoclonal antibody, with no increased bleeding risk [117]. This evidence concerns the gene CLEC1B and Sepsis.