In ICC, the inactivation of p53 has been implicated in various studies.[43] It has been reported that miR‐191 could downregulate TET1 levels, leading to p53 gene TSS staying methylated and thereby promoting ICC progression.[17] Given that p53 is the most frequently mutated gene in human cancers, targeting p53 has emerged as an attractive approach for anti‐tumor therapy. This evidence concerns the gene TET1 and neoplasm.