Recently, much interest have been focused on the role of INI-1, a partner gene of transfusion protein All-1 for leukemogenesis of acute leukemia cases.
Thus a single mutated ALL1 allele with the partial tandem duplication is sufficient for ALL1-associated leukemogenesis, irrespective of the number of normal genes present.
Partial duplication of ALL-1, in which a portion of a putative protooncogene is fused with itself, represents an additional genetic mechanism for leukemogenesis.