The rationale for studying the inflammation-mediated carcinogenesis arises from the evidence that chronic inflammation is a known unfavorable condition, which predisposes to the onset of cancer; moreover, most solid tumors are characterized by an intrinsic tumor-promoting inflammatory response.41 For example, Rokavec and colleagues reported a feedback loop among Interleukin (IL)-6, STAT3 and miR34a, able to increase the invasiveness of colorectal cancer (CRC) cells.42 In a mouse model of colon cancer, the overexpression of IL-8 induces cancer growth and metastatization.43 The gene discussed is STAT3; the disease is cancer.