This results in reduced p62 expression, leading to the further disruption of redox homeostasis through the inactivation of NRF2.[82] Mutations in p62 are associated with neurodegenerative diseases ALS and frontotemporal lobar degeneration (FTLD),[44] including in the KIR region.[83] These disease‐linked mutations disturb selective autophagy and NRF2‐mediated anti‐oxidative stress responses,[84] further supporting the link between disruption of NRF2 activation via p62 and neurodegeneration. The gene discussed is SQSTM1; the disease is frontotemporal dementia.