In NB, multiple defects in mediators of apoptosis have been described and, among them, the increased expression of antiapoptotic molecules such as Bcl-2 (Castle et al, 1993) and the decrease sensitivity to tumour necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis secondary to the inactivation of caspase 8 (Hopkins-Donaldson et al, 2000; Teitz et al, 2000) appear to be the most consistent findings in aggressive tumours. The gene discussed is BCL2; the disease is neoplasm.