Multiple pathways have been found involved in regulation of c‐MYC expression, such as ERK, Wnt‐β‐catenin, TGFβ‐Smad3, and Notch1 pathway.[39] We checked the change of these pathways in tumor cells after I3A treatment and found that only the level of phosphorylated ERK (p‐ERK) was significantly decreased upon I3A treatment, and changes of p‐ERK and c‐MYC levels showed similar patterns in tumor cells after I3A treatment (Figure S8C,D, Supporting Information), suggesting that p‐ERK may mediate I3A‐induced c‐MYC downregulation. This evidence concerns the gene TGFB1 and neoplasm.