Importantly, nuclear YT (structure formed by the YT521-B protein) bodies that contain the YTHDC1 reader protein were already discovered in the late 1990s.98 YTHDC1-deficient leukemia cells exhibited significantly delayed disease development in patient-derived xenotransplantation models of AML.12 Interestingly, Glu-rich N-terminal and Arg-Pro-rich C-terminal IDRs of YTHDC1 facilitated its nuclear compartmentalization in AML cells, but no such condensates were found in cord blood-derived CD34+ cells that generally express lower levels of YTHDC1. This evidence concerns the gene CD34 and acute myeloid leukemia.