Immunotherapies have shown considerable efficacy for the treatment of various cancers, but a multitude of patients remain unresponsive for various reasons, including poor homing of T cells into tumors. In this study, we investigated the roles of the leukotriene B 4 receptor, BLT1, and CXCR3, the receptor for CXCL9, CXCL10, and CXCL11, under endogenous as well as vaccine-induced antitumor immune response in a syngeneic murine model of B16 melanoma. Significant accelerations in tumor growth and reduced survival were observed in both BLT1−/− and CXCR3−/− mice as compared with wild-type (WT) mice. Analysis of tumor-infiltrating leukocytes revealed significant reduction of CD8+ T cells in the tumors of BLT1−/− and CXCR3−/− mice as compared with WT tumors, despite their similar frequencies in the periphery. Adoptive transfer of WT but not BLT1−/− or CXCR3−/− CTLs significantly reduced tumor growth in Rag2−/− mice, a function attributed to reduced infiltration of knockout CTLs into tumors. Cotransfer experiments suggested that WT CTLs do not facilitate the infiltration of knockout CTLs to tumors. Anti–programmed cell death-1 (PD-1) treatment reduced the tumor growth rate in WT mice but not in BLT1−/−, CXCR3−/−, or BLT1−/− CXCR3−/− mice. The loss of efficacy correlated with failure of the knockout CTLs to infiltrate into tumors upon anti–PD-1 treatment, suggesting an obligate requirement for both BLT1 and CXCR3 in mediating anti–PD-1 based antitumor immune response. These results demonstrate a critical role for both BLT1 and CXCR3 in CTL migration to tumors and thus may be targeted to enhance efficacy of CTL-based immunotherapies.