Physicians have been acquainted with the seemingly incongruous association of situs inversus with bronchiectasis for a century.1,2 Primary ciliary dyskinesia has been identified as the underlying cause of bronchiectasis and its accompanying maladies: sinusitis, hearing loss, and infertility in men and women (sperm and oviduct immotility) with Kartagener syndrome. Less well known is that a deficit in embryonic ciliary motility may result in situs errors and heterotaxy as quantified by Shapiro et al3 in this issue of CHEST (see page 1176). Cartwright et al4 demonstrated the mechanism whereby cilia determine left-right asymmetry. Slough et al5 delineated their cardiac role in mouse embryos with absent cilia in which endocardial cushions failed to develop, leading to heterotaxy. They suggested that cardiac cilia function as mechanosensors, integrating flow, cardiac function, and morphogenesis. This conceptual framework is both scientifically gratifying and a tribute to the generative power of natural selection, which has led to the varied and invaluable adaptive repurposing of the primitive mechanism of ciliary motility. Do the authors agree with this unifying formulation of the genesis of the multifarious features of Kartagener syndrome?