The article (press release?) left me extremely baffled about the paper's contribution. (The title is… obvious? I'd worked it out a priori, and I don't even work

The article (press release?) left me extremely baffled about the paper's contribution. (The title is… obvious? I'd worked it out a priori, and I don't even work in this field!) The paper's "eLife assessment" (apparently a form of peer review) cleared it up: https://elifesciences.org/articles/99602 https://elifesciences.org/articles/99602 > These conclusions could largely have been predicted by extrapolating from previous findings in the field, but nevertheless demonstrating them directly is a fundamental advance. The contribution of this paper is a dataset and a methodology, which the abstract describes: > Here, we investigate sex-biased gene expression and micro-evolutionary patterns of these genes in populations of subspecies and species of wild mice (genus Mus) that were raised under controlled conditions. […] Comparison with data from humans shows mostly fewer sex-biased genes compared to mice and strongly overlapping SBI distributions between the somatic organs of the sexes. We conclude that adult individuals are composed of a mosaic spectrum of sex characteristics in their somatic tissues that should not be cumulated into a simple binary classification. which seems a clearer description, more appropriate to layfolk, than the article. The article also claims: > This also means: mouse models are of very limited use when applied to sex-specific medicine in humans. which the paper doesn't say. The paper does say: > The fast evolution of sex-biased expression is also a warning sign that mouse models may not be suitable for developing gender-specific medicinal treatments for humans, especially in view of the fact that humans have a much less sex-biased transcriptome than mice. (That doesn't mean the article's claim isn't true, but press release articles shouldn't draw conclusions not present in their source material!) We're well outside my domain of expertise, but the paper says: > All of the SBI distributions are more or less overlapping between males and females, including breast tissue, similar to that in mouse. and we know that most sexual dimorphism in humans is governed by the endocrine system (including in breast tissue), and that isn't necessarily directly linked to gene expression (though it often is); so I suspect there are actually plenty of ways in which mouse models can be usefully applied to sex-specific medicine in humans. What they have done here is described a limitation (or, I suppose, a family of limitations), not concluded that the limitations are "very". Indeed, the final sentence of the conclusion is: > It will therefore be interesting in the future to focus on their roles in generating the differences between the somatic sexual phenotypes in given species.