This selection was based on the high abundance of HDAC2 and previous studies reporting that HDAC2 regulates the transcriptional activity of SMAD3 to maintain the tumorigenic potential of brain tumor stem cells (BTSCs).[20] Co‐IP experiments verified that endogenously expressed PJA2 and HDAC2 could interact with each other in SW480 and DLD‐1 cells (Figure S7C,D, Supporting Information). This evidence concerns the gene SMAD3 and brain neoplasm.