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. The gene discussed is TP53; the disease is neoplasm.