Approaches that have been studied in CLL include those that bypass nonfunctional p53 by acting downstream of p53 to regulate genome maintenance activities (e.g., cyclin-dependent kinase (CDK) inhibitors), and others that seek to structurally alter mutant p53 or otherwise attempt to deplete it (e.g., PRIMA-1 and HSP90 inhibitors, respectively). The gene discussed is TP53; the disease is B-cell chronic lymphocytic leukemia.