In support of the biological impact of these mutated genes in CLL, (1) Analysis of mutated patients exhibit an enrichment of gene sets associated with transcriptional activation of the MAPK-ERK pathway [44], (2) preliminary in vitro analysis suggests cells from these patients are prone to killing with ERK inhibitors [45], (3) BRAF mutations accelerated disease progression in Eμ-TCL1 mice [46], (4) mutant BRAF has been implicated in venetoclax resistance [47], and (5) KRAS mutated cases associated with poor response to chemoimmunotherapy [27] and lenalidomide [48]. This evidence concerns the gene KRAS and B-cell chronic lymphocytic leukemia.