Unlike tumor-suppressive apoptosis or autophagic cell death, necrosis has been implicated in tumor progression and aggressiveness by releasing a nuclear protein, high mobility group box 1 (HMGB1), that is normally involved in DNA bending and acts as a transcriptional regulator in nuclei but exerts tumor-promoting cytokine and angiogenic activities when released into the extracellular space during necrosis [1]–[6]. The gene discussed is HMGB1; the disease is neoplasm.