Our results support that, by fuelling intestinal inflammation, S100B can build a pro‐malignant microenvironment that initiates tumour growth, as supported by the evidence that long‐standing UC is one of the best‐recognized predisposing factors to colon carcinogenesis.2, 36 In our study, the up‐regulation of S100B orchestrates an increase in oxidative stress and nitric oxide (NO) production, through the increased expression of iNOS. This evidence concerns the gene S100B and neoplasm.