CLEC1B and congenital vertical talus: Similarly, mice depleted of CLEC-2 (ref. 9) or expressing CLEC-2 with a mutated, signaling-dead hemITAM in blood cells (Clec1bY7A/Y7A)16 or lacking spleen tyrosine kinase (Sykfl/fl, Pf4-Cre)17, an essential component of the CLEC-2-ITAM signaling pathway, were resistant to INU1-fab-induced platelet consumption, neurological impairment and lethality (Extended Data Fig. 5) demonstrating a key role of CLEC-2/ITAM signaling for the pathogenesis of CVT in these animals.