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. The gene discussed is HSP90AB1; the disease is amyotrophic lateral sclerosis.