Though CLIP-170 is involved in cytoskeleton arrangement, male mice with disruption of CLIP-170 exhibited abnormal sperm and reduced fertility without skeletal phenotypes,65 whereas Lrrk1-deficient males showed normal fertility but severe osteopetrosis.3 A nonsense mutation in the human CLIP-170 gene caused the absence of CLIP-170 transcripts and protein, resulting in an autosomal recessive intellectual disability without radiographically detectable skeletal abnormalities66 (and personal communication). This evidence concerns the gene LRRK1 and osteopetrosis.