Aberrant splicing and reduced stathmin 2 levels seem to be a major feature of sporadic and familial cases of ALS (except those with SOD1 mutations)3,4 and in frontotemporal lobar degeneration (FTLD) due to TDP-43 proteinopathy11 (FTLD-TDP). This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.