As a result, netrin-1 overexpression and/or the decrease in DCC or UNC5H have been described as a mechanism for cancer cells to inhibit proapoptotic signalling pathway, either through the autocrine loop of netrin-1, interaction of netrin-1 with its dependence receptor or through the absence of the dependence receptors, to promote cancer cell survival and thus increase cancer cell viability and migration [19]. This evidence concerns the gene DCC and cancer.