The immunophilin FK506-binding protein 51 (FKBP5) modulates inflammation through NF-κB signalling,52,53 and forms a chaperone complex with a heat shock protein (HSP90) in response to stress.54 We interrogated whether this was also the case in C9-ALS-FTSD brain tissue by using immunohistochemistry, rather than in situ hybidization, as the functional form of NF-κB is a protein whose cellular localization and expression level determines its function. The gene discussed is C9; the disease is amyotrophic lateral sclerosis.