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After birth, the availability of oxygen and nutrients to organs and tissues changes. This invokes changes in metabolism. Gong\n            <jats:italic>et al.<\/jats:italic>\n            studied the developmental transitions in mouse heart mitochondria soon after birth. Mitochondria were replaced wholesale via mitophagy in cardiomyocytes over the first 3 weeks after birth. Preventing this turnover by interfering with parkin-mediated mitophagy specifically in cardiomyocytes prevented the normal metabolic transition and caused heart failure. Thus, the heart has coopted a quality-control pathway to facilitate a major developmental transition after birth. Wai\n            <jats:italic>et al.<\/jats:italic>\n            examined the role of mitochondrial fission and fusion in mouse cardiomyocytes. Disruption of these processes led to \u201cmiddle-aged\u201d death from a form of dilated cardiomyopathy. Mice destined to develop cardiomyopathy were protected by feeding with a high-fat diet, which altered cardiac metabolism.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Science<\/jats:italic>\n            , this issue p.\n            <jats:related-article xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" related-article-type=\"in-this-issue\" xlink:href=\"10.1126\/science.aad2459\">10.1126\/science.aad2459<\/jats:related-article>\n            , p.\n            <jats:related-article xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" related-article-type=\"in-this-issue\" xlink:href=\"10.1126\/science.aad0116\">10.1126\/science.aad0116<\/jats:related-article>\n            ; see also p. 1162\n          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