To further explore whether SETDB1 increased MCT1 protein expression, we transfected different SETDB1 overexpression plasmids into CRC cells and found that only overexpression of wild‐type (WT) SETDB1, but not the SETDB1 H1224K mutant deficient for methyltransferase activity,[24] significantly enhanced the expression of MCT1 protein, whereas changes in MCT1 mRNA were insignificant (Figure 1i,j and Figure S1c,d, Supporting Information). This evidence concerns the gene SLC16A1 and colorectal carcinoma.