Finally, using CLL-like cells transfected with the mutated NOTCH1 intracellular domain (NICD-mut) we constructed a putative model for CD20 downregulation in NOTCH1 mutated CLL whereby the truncated PEST domain of NICD-mut demonstrated increased affinity for RBPJ, thus tilting the balance between activation and repression complexes towards the former and allowing histone deactylase (HDAC) from the repression complex to freely migrate to other parts of the genome including the promotor of the CD20 gene leading to downregulated transcription and CD20 expression [81]. Here, RBPJ is linked to B-cell chronic lymphocytic leukemia.