Studies have reported that: 1) the levels of CMTM5-v1 in the malignant tissues of patients with prostate cancer are lower than the levels in their  nearby normal prostate gland tissues as well as in the tissues of patients with benign prostate hyperplasia; 2) patients with lower prostate cancer tissue levels of CMTM5-v1 have higher prostate cancer Gleason scores and therefore poorer prognoses than patients with higher prostate cancer tissue levels of CMTM5-v1; and 3) the forced overexpression of CMTM5-v1 in cultured DU145 cells (a human prostate cancer cell line) reduces, while the forced higher expression of the CMTM5-v1 levels increases, their proliferation and migration. Similar findings for an unspecified CMTM5 isoform are reported in ovarian cancer, hepatocellular carcinoma, pancreatic cancer, non-small-cell lung carcinoma, renal cell carcinoma, and breast cancer. The forced over expression of CMTM5-v1 in Huh7 human hepatic cells also inhibited the ability of these cells to grow in a mouse model of cancer. Finally, various cancer human cell lines including those of the liver, breast, prostate, colon, stomach, nasopharynx, laryngopharynx, esophagus, lung, and cervix express low levels of, or no, CMTM5-v1 and concurrently have highly methylated CpG sites near to the CMTM5 gene. These findings suggest that the CMTM5 gene may act as a tumor suppressor gene, i.e. a normal gene whose product(s) inhibit the development and/or progression of various cancers. The findings also support further studies to confirm and expand these relationships and determine if the expression of CMTM5 isoforms can be used as tumor markers for these cancers severities/prognoses and/or targets as for treating them.