In contrast, the ability of both MLL-ENL, a t(11;19) translocation in infant acute leukemias, and MOZ-TIF2, an AML inversion of (8)(p11q13), fusion oncogenes to restore self-renewal ability to previously-committed progenitors that normally lack the capacity to self-renew, and evidence of AML LSCs derived from the CD34− fraction [150] provide an alternative origin of the LSC [151,152]. This evidence concerns the gene MLLT1 and acute myeloid leukemia.