Immune checkpoint blockade therapy is based on the inhibition of the tumor-mediated suppression of anticancer immune responses. However, the efficacy and effectiveness of said therapy vary greatly across individual patients and among different tumor types. A substantial unmet need is thus to identify novel targets that can enhance the therapeutic efficacy of the immune checkpoint blockade therapy. S1P is produced by sphingosine kinases (i.e. SK1 and SK2) that catalyze the phosphorylation of sphingosine to S1P. SK2 inhibitors were described as suitable for the treatment of cancer. However the role of SK2 in the immune tumor microenvironment has never been investigated. The inventors now showed that genetic deletion of SPHK2 leads to a delay in the melanoma tumor growth and an increase in tumor-infiltrating effector lymphocytes. In particular the increase of tumor-infiltrating effector lymphocytes in the tumor is associated with a decrease in the amount of tumor-infiltrating myeloid-derived suppressor cells. Moreover, the combination of SPHK2 deficiency with immune-checkpoint blockade leads to tumor rejection and increases survival rate. Accordingly, the present invention relates to use of SK2 inhibitors in combination with immune checkpoint blockade therapy for the treatment of cancer.L'invention concerne une thérapie de blocage de point de contrôle immunitaire fondée sur l'inhibition de la suppression médiée par une tumeur de réponses immunitaires anticancéreuses. Cependant, l'efficacité et l'efficience de ladite thérapie varient fortement sur l'ensemble des patients individuels et selon différents types de tumeurs. Il existe donc un besoin insatisfait d'identifier de nouvelles cibles qui peuvent améliorer l'efficacité thérapeutique de la thérapie de blocage de points de contrôle immunitaire. S1P est produite par des sphingosine kinases (c'est-à-dire SK1 et SK2) qui catalysent la phosphorylation de la sphingosine en S1P. Des inhibiteurs de SK2 ont été décrits comme
