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<jats:title>For HIV: Location, location, location</jats:title> <jats:p> HIV-infected cells linger even in the face of therapy, and this persistence, termed the latent reservoir, is a major hurdle for curing HIV. HIV integrates itself into the DNA of its host cells. Could that affect the latent reservoir? To find out, Maldarelli <jats:italic>et al.</jats:italic> drew blood from five HIV patients on antiretroviral therapy and analyzed sites where HIV had inserted itself into the blood cells' DNA (see the Perspective by Margolis and Bushman). In many cases, these sites were not random; HIV often weaseled its way into genes that help cells grow and proliferate. Where HIV integrates into the host genome may thus determine the size of the latent reservoir. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6193" page="179" related-article-type="in-this-issue" vol="345" xlink:href="10.1126/science.1254194">179</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6193" page="143" related-article-type="in-this-issue" vol="345" xlink:href="10.1126/science.1257426">143</jats:related-article> </jats:p>