REEP1 and hereditary spastic paraplegia: As reported previously, REEP1 WT/KO and REEP1 KO/KO mice develop a spastic gait disorder and degeneration of corticospinal axons compatible with HSP in a gene‐dosage‐dependent manner.[23] To study the pathophysiology of REEP1‐associated dHMN, we now modeled the deletion of exon 5 in mice, which is caused by the splice‐site mutation c.304‐2A>C.[23] For targeting, we inserted a loxP site into intron 4 and a Neomycin selection cassette flanked by loxP sites into intron 5.