At any rate, the manifestation of CNS and especially motor neuron specific pathology due to a mutation in DnaJC11 surely opens new possibilities for the search of novel contributors in neuromuscular diseases, particularly in conditions with motor neuron involvement like ALS, and especially in the light of our finding that expression of huDNAJC11 can fully compensate the depletion of muDNAC11. The gene discussed is DNAJC11; the disease is amyotrophic lateral sclerosis.