More work has to be performed to prove that the effect seen in netrin-1-overexpressing mice is indeed due to the inhibition of DCC- or UNC5H-induced cell death by netrin-1 and not to the fact that netrin-1 overexpression leads to overstimulation of alternative receptors, such as integrins or A2b, nor to the fact that netrin-1 has a positive effect on tumour development due to chemoattrative/chemorepulsive activities. The gene discussed is NTN1; the disease is neoplasm.