The loss of the PML (Acute Promyelocytic Leukemia Inducer; OMIM 102578) interaction domain, which extends from amino acid (aa) 1517 to 1741, as well as of two different RUNX1-2 domains (extending from 1517–1642 aa and 1913–1948 aa), required for RUNX1-2 protein interaction and activation, are caused by the deletion of the carboxy-terminal portion (Figure 2). The gene discussed is RUNX1; the disease is acute promyelocytic leukemia.