The JNK proteins are activated by multiple and diverse stimuli, leading to varied and seemingly contradictory cellular responses. In particular, JNKs have been reported to have a role in the induction of apoptosis, but have also been implicated in enhancing cell survival and proliferation. Thus the JNK proteins seem to represent an archetype of contrariety of intracellular signaling. The opposing roles of JNKs have been attributed to the observation that JNKs activate different substrates based on specific stimulus, cell type or temporal aspects. Because of their analogous expression in apparently almost every tissue, JNK1 and JNK2 have most often been considered to have overlapping or redundant functions. In spite of this assessment, research evidence suggests that the functions of JNKs should be addressed in a manner that differentiates between their precise contributions. Specifically in this review, we examine evidence regarding whether the JNKs proteins might play distinctive roles in cellular processes associated with carcinogenesis.