ANXA11 and amyotrophic lateral sclerosis: Disease‐associated mutations, such as R235Q, are observed in the C‐terminal core domain: a variant of AnxA11 R235Q overexpressed in mouse primary motor neurons and human embryonic kidney (HEK) 293 cells was shown to produce high–molecular weight insoluble species able to sequester wild‐type AnxA11 similar to those observed in ALS patients [80].