As opposed to the effect of prenatal infection and direct maternal injection of IFNγ on hematopoiesis in situ, adoptive transfer assays revealed disparate responses of two fetal HSC populations differentiated by the FlkSwitch model: the Tom+ HSC as a more “conventional” putative adult HSC precursor, and the GFP+ Flk2‐marked HSC as a transient, lymphoid‐biased HSC that functions to give rise to innate‐like lymphocytes during fetal development (Beaudin et al, 2016). Here, PRPF6 is linked to infection.