Finally, to study the mechanisms of the p97 complex and its adaptors during the disease, the mouse model presenting the R155H mutation, found in some patients with ALS, could be used, also to see whether—as happens for the A232E mutation present in the inclusion‐body myopathy with Paget's disease of the bone and frontotemporal dementia—such mutation increases the affinity of p97 for Nploc4. The gene discussed is NPLOC4; the disease is frontotemporal dementia.