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These HTLV-1-infected cells typically have phenotypes similar to that of CD4<jats:sup>+<\/jats:sup>T cells, but the cell status is not well understood. To extract the inherent information of HTLV-1-infected CD4<jats:sup>+<\/jats:sup> cells, we integratively analyzed the ATAC-seq and RNA-seq data of the infected cells. Compared to CD4<jats:sup>+<\/jats:sup>T cells from healthy donors, we found anomalous chromatin accessibility in HTLV-1infected CD4<jats:sup>+<\/jats:sup> cells derived from ATL cases in terms of location and sample-to-sample fluctuations in open chromatin regions. Further, by focusing on systematically selected genes near the open chromatin regions, we quantified the difference between the infected CD4<jats:sup>+<\/jats:sup> cells in ATL cases and healthy CD4<jats:sup>+<\/jats:sup>T cells in terms of the correlation between the chromatin structures and the gene expressions. Based on a further analysis of chromatin accessibility, we detected <jats:italic>TLL1<\/jats:italic> (Tolloid Like 1) as one of the key genes that exhibit unique gene expressions in ATL cases. A luciferase assay indicated that TLL1 has an isoform-dependent regulatory effect on TGF-<jats:italic>\u03b2<\/jats:italic>. 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