While the PFN1 R136W, Q139L and A20T mutations were detected in single individuals with sporadic or familial ALS, respectively [11, 12], pathogenicity of the PFN1 T109M mutation is supported by co-segregation with the disease in the affected family [10] as well as serum microRNA profiles of pre-clinical mutation carriers that are highly similar to profiles of pre-clinical carriers of ALS associated mutations in C9orf72 or SOD1 [14]. Here, PFN1 is linked to amyotrophic lateral sclerosis.