PODXL and esophageal cancer: Using an exemplary target gene PODXL (podocalyxin-like), the authors demonstrated that the ADAR2-regulated recoding editing at codon 241 (His to Arg) confers a loss-of-function phenotype that neutralizes the tumorigenic ability of the unedited PODXL. Qin et al. reported the overexpression of ADAR1 in primary esophageal cancer cell line due to gene amplification [43].