These may include the dysregulation of tau, potentially resulting in the accumulation of TDP-43 through the inhibition of proper HSP90AB1 function, destabilization of interactions with other J proteins involved in neuroprotection, or the inability to accurately chaperone the variety of Hsp70s or Hsp90s involved in ALS-associated protein aggregates; although, other potential mechanisms cannot be ruled out. This evidence concerns the gene TARDBP and amyotrophic lateral sclerosis.