Active β-catenin-TCF/LEF signaling drives expression of the G-CSF receptor on HSPCs which, in turn, renders HSPCs more responsive to G-CSF thereby promoting steady-state and emergency granulopoiesis (left panel). By contrast, disruption of the β-catenin-TCF/LEF signaling results in impaired steady-state and emergency granulopoiesis (right panel). See graphical abstract in the article by Danek et al that begins on page 2574.