Ras-driven tumours also showed a slight retardation in tumour development with the addition of aPKCCAAXDN, although this was much less striking than the effects with N. As JNK signalling remains activated in scrib mutant clones expressing aPKCCAAXDN, it is likely that JNK can restrain NACT-driven tumour overgrowth, and RasACT is more effective than NACT at counteracting such a JNK-mediated restraint. Here, MAPK8 is linked to neoplasm.