Microdeletions in the 12q32 site including the HOXC cluster and other adjacent genes results in significant disruption of normal cell function48–50, and amplification of the 8q22 site including EDD1 and GRHL2 genes, negative regulators of apoptosis, have been described in breast, pancreas, and lung cancer cells as a mechanism for evasion of death receptor-activated therapies51. The gene discussed is UBR5; the disease is lung cancer.