Moreover, the hTBK1-c.978T>A mutation significantly increased KEAP1 expression and inhibited Nrf2 signaling in NSC-34 cells, and these effects were partially reversed by knocking down p62.458 These results suggest that the hTBK1-c.978T>A mutation induces ferroptosis via the KEAP1/Nrf2/p62 signaling pathway, pointing to a possible new target for ALS. The gene discussed is KEAP1; the disease is amyotrophic lateral sclerosis.