This phenomenon may be partially attributable to limited sample size, but the more critical underlying mechanism likely involves c-Myc/Bcl-2-driven metabolic reprogramming potentially operating partially independent of proliferation regulation pathways—meaning the tumor cells’ survival advantage may be preferentially achieved through energy metabolism pathways, where proliferative activity in specific DEL subtypes could be masked by metabolic dysregulation. The gene discussed is MYC; the disease is neoplasm.