Promoter CpG island hypermethylation is a common strategy for cancer cells to silence tumor-suppressor gene expression, thereby facilitating the initiation and progression of cancer. Many cancers acquire a so-called CpG island methylator phenotype (CIMP), characterized by the simultaneous occurrence of multiple aberrantly hypermethylated gene promoters. Mechanisms underlying CIMP have generated a considerable interest in the recent years. Common in many tumors with CIMP is the deregulation of 5mC-directed DNA hydroxylase activity provided by TET proteins. Colon cancers with an activating BRAFV600E mutation display extensive CGI hypermethylation and transcriptional silencing of many genes, including TET proteins. However, the causal link between BRAFV600E, TET proteins regulation and DNA hypermethylation has not been established. We show here stably expressing BRAFV600E in colon cancer cell line that BRAFV600E at first regulates the expression of TET1 independent of its own promoter methylation. The downregulation of TET1 is enough to establish hypermethylation at several CIMP targets. We further show that pharmacological inhibition of BRAFV600E is able to reverse the hypermethylation phenotype. Our work demonstrates, for the first time, a direct functional link between BRAF signaling and TET1 action and shows that TET1 downregulation is required for BRAF-induced DNA hypermethylation in colon cancer.