Like Sly, Xmr and its close relatives are highly expressed in spermatids [37], and our recent finding that a major transcriptional consequence of MSYq deficiency is the upregulation of a number of spermatid-expressed X genes, including Xmr, leads us to suspect that amplification of Xmr and Sly is a result of 'genomic conflict' between sex linked meiotic drivers and suppressors [37,38]. Here, SASH3 is linked to hyperinsulinemic hypoglycemia, familial, 4.