It was reported that DC-intrinsic XBP1 promotes ovarian cancer progression and that silencing XBP1 in DCs enhances T cell antitumor immunity.31 XBP1 also enhances the expression of T cell exhaustion markers such as PD-1, TIM-3 and Lag3 in CD8+ T cells during infection,20 32 and the activation of XBP1 in T cells was associated with the suppression of mitochondrial activity and reduced IFN-γ, TNF-α and granzyme B production.20 33 Therefore, functions of immune cells, including CCL4 production, are regulated by ER stress, which can be a therapeutic target. This evidence concerns the gene HAVCR2 and infection.