MAPK11 and peripheral neuropathy: Interestingly, viable M. leprae appeared to modulate genes related to Schwann cell plasticity and dedifferentiation, such as BDNF, cJUN, SOX10, ERBB2, and MAPK11. In summary, this first set of analysis points to the notion that dead M. leprae induces greater expression of peripheral neuropathy and nerve regeneration support genes whereas viable M. leprae acts by modulating genes related to Schwann cell plasticity and dedifferentiation.