HnRNP K has also been identified as a key driver for nuclear retention of long non-coding RNA (lncRNA) Malat1 which, when disrupted, leads to increased Malat1-TDP-43 binding and an increased propensity for TDP-43 aggregation as has been observed in ALS patients [54, 62]. This evidence concerns the gene MALAT1 and amyotrophic lateral sclerosis.