Hypothetical model of the mechanisms involved in regulation of Aiolos transcription and consequence of its overexpression on the cell survival in leukemogenesis of CLL. The chromatin status at the Aiolos promoter in CLL is defined by the demethylation of DNA and an enrichment of euchromatin associated histone markers, compared with normal B cells. These epigenetic modifications should allow its upstream effectors, such as NF-κB, constitutively activated in CLL, to gain access to promoter, resulting overexpression of Aiolos. Ikaros does not seem deregulated at its expression level in CLL. This Aiolos deregulation could participate in the survival of cells from CLL patients.