For example, emerging preclinical studies indicate that HDIVC could display increased effectiveness in cancers with mutations in KRAS, BRAF, TET2, IDH1, IDH2, VHL, FH, or SDH and in those with mismatch repair deficiencies or high expressions of GLUT1, and at least some of these gene mutations are associated with prostate cancer (32–36). This evidence concerns the gene TET2 and prostate cancer.