The team hoped to use the splicing defects they identified in the mRNA targets of hnRNP H to create a ‘signature’ that would help them identify which cases are caused by mutations in C9orf72. To begin, they studied 18 of these targets in 50 postmortem samples from the brains of people with ALS, FTD, or both. Here, C9orf72 is linked to amyotrophic lateral sclerosis.