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This phenotype is driven by the failure of CUL5 to negatively regulate IL-3-induced STAT5 signaling via the CRL5-LRRC41 complex, which is essential for maintaining HSC quiescence and lineage balance

Latest research has however questioned its reliability as thiamine transporters THTR1 and RFC1 in erythrocytes are upregulated in thiamine deficieny and RBC TK levels are not decreased in tandem [183]