NDRG1 is overexpressed in some cancer cells such as colorectal and breast cancer cell lines. Analysis of clinical samples from cancer patients showed that NDRG1 (N-myc downstream regulated gene-1) acted as a tumor suppressor in those cancer cells, and the low expression was correlated with shorter survival. On the other hand, it has been reported that overexpression of NDRG1 upregulates the expression of ATF3 (activating transcription factor 3), which is a stress-inducible gene, and thereby promotes tumor progression and metastasis. Taken together, the molecular mechanism of NDRG1 in cancer is still controversial and needs to be unveiled. Moreover, a role of NDRG1 in lymphocytes is completely unknown. We investigated the correlation between expression of NDRG1 and over-all survival in various types of cancers. In many cancers, NDRG1 is positively correlated with poor prognosis, but not in glioblastoma. We searched candidates that regulate immune functions specific in tumor-infiltrating lymphocytes by NGS using a mouse model and identified NDRG1 acts as an immune-related protein involved in the recruitment of tumor-infiltrating lymphocytes to the tumor microenvironments. Subsequently, we expressed NDRG1 in cancer cells and analyzed the effects on the tumor microenvironments. We are currently analyzing the detailed molecular mechanism of NDRG1 in tumor-infiltrating lymphocytes.