This would be due to hyposialylation status, because: (1) patients with disease-causing variants in GNE or SLC35A1 involved in a sialylation pathway also often exhibit thrombocytopenia, in association with an exaggerated platelet clearance in the liver14–16; and (2) removal of sialic acids from platelets by neuraminidase treatment has resulted in shortened platelet life, in association with elevated serum PAIgG levels in baboons17. This evidence concerns the gene SLC35A1 and Thrombocytopenia.