Furthermore, primary human fetal liver CD34+ HSPCs were gene edited using CRISPR-Cas9 to produce HSPCs carrying a t(4;11)/KMT2A/AFF1 translocation; they were shown to drive fetal specific and infant ALL molecular programs and to recapitulate clinical characteristics of the human disease (including treatment resistance and CNS disease) in an NSG xenograft model of infant ALL [183], providing support for their hypothesis. The gene discussed is AFF1; the disease is acute lymphoblastic leukemia.