Alfredsson et al. (2014) demonstrated that EA induced caspase 9 and caspase 3 activation in human neuroblastoma cells, resulting from increased mitochondrial membrane permeability in a dose- and time-dependent manner. Similarly, Larrosa et al. (2006) reported that Caco-2 cells induced caspase 9 as the initiator caspase and caspase 3 as the effector caspase. Li et al. (2005) reported that EA application to a bladder cancer cell line did not affect the level of caspase 8 and that caspase 8-independent apoptosis occurred. The gene discussed is CASP3; the disease is neuroblastoma.