IL-3 does not readily cross the blood brain barrier, and increasing the IL-3 brain presence via intrathecal delivery of recombinant IL-3 only appears to be beneficial when endogenous IL-3 had been ablated.1 Also, this study uses a model of AD (the so-called 5xFAD-mouse-model, harboring 3 pathogenic mutations in APP and 2 pathogenic mutations in PSEN1, but no mutation in MAPT), which does not faithfully recapitulate the typical TAU pathology crucial for human disease. Here, IL3 is linked to Alzheimer disease.