Such oxidative stress conditions facilitate tumor growth in multiple ways by causing DNA damage and genomic instability and ultimately, by reprogramming cancer cell metabolism.39 Zhang et al. showed that the stemness of pancreatic cancer cells was promoted through the Nox/ROS/NF‐κB/STAT3 signaling cascade.26 The S100A9 protein in exosomes from chronic lymphocytic leukemia cells promotes NF‐κB activity during disease progression.40 Our results also showed that S100A9 enhanced the phosphorylation of STAT3 and NF‐κB in colon cancer cells. This evidence concerns the gene STAT3 and colonic neoplasm.