This was also seen in relapsed disease, where TNFα and NFκB associated pathways were upregulated; in addition, regulators of RNA splicing, such as SRSF1, and apoptosis, such as MCL1, were higher expressed than at pre-treatment, indicating a possible biological role in driving CLL progression after therapy. This evidence concerns the gene NFKB1 and B-cell chronic lymphocytic leukemia.