Upon stimulation with Influenza antigens, we uncovered a trend toward higher IFNα-production, a key cytokine whose chronic activation impairs hematopoietic stem cells (HSCs) in mice, while acute exposure can lead to activation and proliferation of dormant HSCs and early progenitor cells.15 IFNα also activates JAK-STAT-signaling, a crucial pathway in the development of BCP-ALL whose timely inhibition may even prevent the development of BCP-ALL in mouse models with genetic leukemia predisposition.2 The gene discussed is SOAT1; the disease is acute lymphoblastic leukemia.