HSC contribution to B1a cells. All definitive HSCs, by definition, are capable of long-term multilineage contribution to the 5 main lineages of mature cells in adult recipients. Accumulating evidence converges on the concept that adult HSCs are poorer producers of B1a cells compared with fetal HSCs. Fetal HSC heterogeneity, which can be separated retrospectively by functional lineage bias classification,²⁵  prospectively by surface markers^24,26,32  or by lineage tracing,³²  supports the notion that some fetal HSCs are more B1a competent than others and that transiently existing fetal HSCs account for most of the B1a capability. The HSC contribution to B1a cells emphasized here does not exclude the possibility that cells without robust engraftment capability (“pre-HSCs”) also contribute to the B1a pool. GM, granulocyte/macrophage; Plts, platelets; RBCs, red blood cells.