Deletion of platelet CLEC‐2 abolished liver thrombosis without altering bacterial count.142 In contrast, the CLEC‐2‐podoplanin axis inhibits inflammation in mouse models of LPS‐induced acute respiratory distress syndrome and cecal ligation and puncture without altering thrombosis.83, 85, 86 The inhibition of CLEC‐2–podoplanin interaction exacerbates the cytokine storm and impairs macrophages recruitment to the infected peritoneum increasing bacterial load. This evidence concerns the gene CLEC1B and acute respiratory distress syndrome.