Prognostic relevance of MYD88 mutations in CLL: the jury is still out

Genome surveys have offered a comprehensive view of the genetic landscape of chronic lymphocytic leukemia (CLL), identifying several recurrently mutated genes, including myeloid differentiation primary response 88 (MYD88). The predominant mutation concerns a p.L265P substitution within exon 5,1,2 which leads to constitutive nuclear factor kappaB stimulation, thus conferring a proliferation and survival advantage to the mutant cells.1 MYD88 mutations reach up to 2% to 5% in CLL and are strikingly enriched among patients expressing mutated IGHV genes (M-CLL).