Even if our study has some limitations, such as the low number of biologic pathways investigated and the small sample size, our data may suggest that the angiogenic (VEGF, PDGFr) and pro-proliferative (TGF-b, STAT3) pathways already supposed to be involved in the pathogenesis of cholesteatomas could be differently modulated/activated in locally more destructive forms, typically found in children (Figure 5). The gene discussed is STAT3; the disease is cholesteatoma.