TP53 and B-cell chronic lymphocytic leukemia: Genomic instability in CLL may be further promoted by permissive genetic contexts resulting from loss of cell cycle control (e.g. TP53 or CDKN2A/B mutation), DNA damage response (DDR; e.g. ATM or SAMHD1 mutation) (75) or telomere maintenance (e.g. POT1 mutation) (76), giving rise to additional genetic heterogeneity.