The transection of nerve fibers evokes a characteristic reaction in the injured neurons, the so-called cell body response (CBR), which comprises aspects of developmental re-differentiation with parallel loss of the transmittory phenotype, efforts or achievement of axonal elongation and re-construction of effective synapses. Neither the signals underlying the onset of CBR nor the programs underlying regeneration are sufficiently elucidated. Here we review the putative role of two subfamilies of the MAP kinases, the JNKs (c-Jun N-terminal kinases) and the p38 kinases in the CBR. Following nerve injury with subsequent CBR, JNKs are rapidly activated and this activation persists for weeks until neu-ronal cell death or successful regeneration. The various functions render JNKs to perfect candidate molecules for the realization of the CBR including axonal transport, activation of c-Jun, modulation of cytoskeletal functions, detection of cytoskeletal alterations, or signal transduction of adhesion molecules in the axon and growth cone. On the other hand, the rapid but transient activation of p38 might interfere with the mitotic arrest, a putative feature of the CBR.