Moreover, melatonin via melatonin receptor MT1 and MT2 can modify the levels of pro- or antiapoptotic proteins such as Bax and Bcl-2 in human neuroblastoma cells [64]; similarly in placenta, treatment with 10 μM of melatonin in villous trophoblast cells increases the survival via inhibition of loss of mitochondrial membrane potential and stimulating the formation of complex Bax/Bcl-2 (intrinsic via), expression of caspase-9, and the activation of ROCK1 [71]. This evidence concerns the gene BAX and neuroblastoma.