Moreover, differently from what is outlined by experimental and clinical data that strongly suggests HRG as a positive contributor to CLD progression (34–36), the few available evidences concerning the role of HRG in carcinogenesis suggests instead HRG as a putative antitumor mediator—for instance, HRG deletion results in enhanced tumor growth and metastatic capacity in mice transplanted with fibrosarcoma or pancreatic carcinoma cells in relation to HRG’s capacity of promoting vessel abnormalities and suppressing antitumor immune responses (37). The gene discussed is HRG; the disease is fibrosarcoma.