Careful examination of the mechanism of action of silibinin on cell signaling elicited by a cytokine mixture (IFNγ + TNF-α) in tumor-derived LM2 mouse lung epithelial cells revealed that its ability to regulate the expression of metalloproteinases and the angiogenesis drivers COX2 and iNOS was causally mediated through impairment of STAT3 activation and nuclear localization [38]. This evidence concerns the gene STAT3 and neoplasm.