The Ikaros family is an important group of transcription factors essential in the normal development of hematopoietic lineages [1, 2, 3]. They function as transcriptional regulators through chromatin remodeling [4] and are active only as dimers [1]. Ikaros family members — Ikaros, Aiolos, and Helios — are DNA-binding, zinc-finger proteins. They all generate a large pattern of splice variants [1,5, 6,7,8]. Cloned Ikaros isoforms are shown in Figure 1. Some of the splice variants lack one or more of the four N-terminal zinc fingers and their DNA binding affinity is altered or totally lost. Isoforms that lack the DNA-binding capacity are thought to have a dominant negative function because they prevent the binding of the dimer to DNA. Ikaros family proteins function as part of a multicomponent chromatin remodeling complex [9]. Splice variants missing one or more exons might selectively lack sites for protein-protein interactions or regulation of the complex, and therefore, have altered function.