SCRIB and neoplasm: These results demonstrate distinct aPKC and JNK-dependent pathways through which loss of Scrib promotes tumourigenesis in Drosophila. aPKC signalling in scrib mutants promotes loss of cell polarity and proliferation, while JNK can either restrain tumour development through cell death or, in cooperation with RasACT or NACT, promote aggressive neoplastic tumour overgrowth.