To test whether Astrin variants are selectively depleted in cancers, we probed the incidence of somatic mutations in Astrin and Ndc80 (an interactor of Astrin)35,38 by comparing multiple tumor tissues for variants in five gene categories: (a) MCPH genes, (b) MVA genes, (c) the Astrin-SKAP complex, (d) Astrin-SKAP interactors, and (e) TP53 and BRCA1 (tumor suppressor genes, as positive controls). This evidence concerns the gene SPAG5 and neoplasm.