The common upregulation of α2,6 sialyltransferases (ST6GALNAC4, ST6GALNAC6), along with NEU1 and NANS in naïve-like CD21low B cells from CVID patients, potentially increases substrate availability through enhanced sialic acid recycling and/or de novo synthesis of CMP-sialic acid (42, 43), suggesting a multifactorial basis for α2,6 hypersialylation in these cells. The gene discussed is NEU1; the disease is common variable immunodeficiency.