 However, the lack of somatic "DCC" mutations made it seem likely that the nearby "SMAD2" and "SMAD4" genes were the reason for 18q21 LOH.The fact that DCC heterozygotes had no increased rates of cancer, even when crossed with mice carrying "Apc" mutations, solidified this viewpoint.The finding that DCC was a receptor for netrin-1 involved in axon guidance initially moved research away from DCC in cancer.