One promising candidate as a potential therapeutic target is Abelson helper integration site-1(Ahi-1/AHI-1) that was identified by retroviral insertional mutagenesis in murine models of leukemia/lymphomas and is highly elevated in certain human lymphoma and leukemia stem/progenitor cells.
A possible explanation for the paradoxical behavior of c-myb was provided by one of the murine T-lymphoma lines bearing an insertion at Ahi-1 (p/m16i) that reproducibly down-regulated c-myb RNA and protein to very low levels or undetectable levels on prolonged culture.