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            <funder>This work was supported by INSERM, Paul Sabatier University, Ligue Nationale Contre le Cancer (LNCC, Equipe Labellisée 2013), INSERM Transfert, Cancéropôle Grand Sud-Ouest, ROTARY Toulouse clubs, Fondation Toulouse Cancer Santé and Fondation ARC (IMMUSPHINX project). The research leading to these results has received funding from the Transcan-2 Research Program, which is a transnational R&amp;D program jointly funded by national funding organizations within the framework of the ERA-NET Transcan-2. C.I. is a recipient of a fellowship from LNCC and Fondation pour la Recherche Médicale (FRM). The IBiSA Toulouse Proteomics facility is supported by the following institutions: Région Midi-Pyrénées, Fonds Européens de Développement Régional, Toulouse Métropole, and the French Ministry of Research with the ‘Investissement d’Avenir Infrastructures Nationales en Biologie et Santé program’ (Proteomics French Infrastructure project, ANR-10-INBS-08). P.B. is supported by the LABEX TOUCAN.</funder>
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                  <biblScope unit="volume">11</biblScope>
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              <p>Immune checkpoint inhibitors (ICIs) have dramatically modified the prognosis of several advanced cancers, however many patients still do not respond to treatment. Optimal results might be obtained by targeting cancer cell metabolism to modulate the immunosuppressive tumor microenvironment. Here, we identify sphingosine kinase-1 (SK1) as a key regulator of anti-tumor immunity. Increased expression of SK1 in tumor cells is significantly associated with shorter survival in metastatic melanoma patients treated with anti-PD-1. Targeting SK1 markedly enhances the responses to ICI in murine models of melanoma, breast and colon cancer. Mechanistically, SK1 silencing decreases the expression of various immunosuppressive factors in the tumor microenvironment to limit regulatory T cell (Treg) infiltration. Accordingly, a SK1-dependent immunosuppressive signature is also observed in human melanoma biopsies. Altogether, this study identifies SK1 as a checkpoint lipid kinase that could be targeted to enhance immunotherapy.</p>
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