First, it has been recently shown that the growth of polarity-deficient scrib or dlg mutant clones is counteracted by the so-called Intrinsic Tumour Suppression (ITS) mechanism, which functions by triggering in the mutant cells both endocytic uptake and endosomal activation of the Eiger protein (homologue of the mammalian Tumour Necrosis Factor), which in turn leads to activation of pro-apoptotic JNK signaling [8,9]. Here, MAPK8 is linked to neoplasm.