FUS and amyotrophic lateral sclerosis: Homozygous FUS P525L mutations in human iPSC-derived microglia have been shown to disrupt transcriptome profiles and alter chemoreceptor signaling, with the upregulation of genes such as P2RY6 and GPR183. These findings are particularly significant as mutations in the FUS gene are a known cause of ALS, contributing to its pathogenesis through both cell-autonomous and non-cell-autonomous mechanisms.