While speculative, the above hypothesis is consistent with the typically slow progression of monoclonal B cell lymphocytosis (MBL) [122,123]; high prevalence of del(13q) in early MBL [124,125]; the better clinical outcome of CLL with del(13q) as the sole chromosomal anomaly [126]; and the progressive appearance of genetic anomalies that alter expression and/or function of p53, either directly (e.g., TP53, ATM, or MDM2) or indirectly (e.g., NOTCH1, SF3B1, BIRC3, and RPS15 [114,125,127-136]. Here, MDM2 is linked to monoclonal B-cell lymphocytosis.