AKT-mediated ERK1/2 activation may rely on its reported ability to inhibit c-Jun N-terminal kinase, which in turn alleviates the repressive function of c-Jun N-terminal kinase on ERK1/2 signaling.31 As many tumor cells have learned to induce ERK1/2 phosphorylation by a MEK1/2-independent signaling route,35 the detailed characterization of the molecular mechanisms allowing for this bypass will be highly relevant. The gene discussed is MAPK3; the disease is neoplasm.