Numerous investigations indicate that CLL relapse is commonly associated with defects in pathways regulating the DNA damage response (in particular, mutations or deletion of the p53 tumour suppressor), inhibition of apoptosis (commonly caused by the overexpression of the BCL-2 family of anti-apoptotic proteins), and RNA metabolism (often affecting the splicing factor 3b subunit 3 -SF3B3-). This evidence concerns the gene BCL2 and B-cell chronic lymphocytic leukemia.