Furthermore, the apparent preferential action of the drug on cycling and recently divided CLL cells suggests that selective MSI2 inhibition would prevent disease progression since these are the fractions of leukemic clones that express the DNA mutator, AID, and hence could develop new DNA abnormalities that might lead to clonal evolution, disease advancement, and clinical deterioration. This evidence concerns the gene AICDA and B-cell chronic lymphocytic leukemia.