Herein we suggest that multiple miRNAs within the 14q32 clusters can target GAB1 in CLL and may explain the difference in BCR signalling capacity and we speculate that the dysregulation of multiple miRNAs could provide precise regulatory control, reduce the degree of redundancy in the epigenetic regulation of key mRNAs, or have an additive impact on transcriptional regulation but these hypotheses remain to be confirmed. This evidence concerns the gene GAB1 and B-cell chronic lymphocytic leukemia.