Oncogenic cooperation in CRC has also been modeled in Drosophila. Cooperation between loss of Apc and hyperactivation of ras (Apc−/−, rasV12), which characterizes malignant stages of human colorectal tumours [140,141], drives the progression of Apc mutant intestinal tumors and the activation of Apc−/−, rasV12 specific transcriptional targets in the Drosophila adult midgut [142,143]. This evidence concerns the gene APC and intestinal neoplasm.