A recent study using post-mortem cortex samples identified three distinct subsets of ALS patients one of which was characterised by de-silencing of multiple families of transposable elements that can be assigned to the groups of both LTR and non-LTR retrotransposons (including L1) and associated with TDP-43 dysfunction (20% of patients) [36]. The gene discussed is TARDBP; the disease is amyotrophic lateral sclerosis.