Figure 4 shows that although p-c-Raf Ser338 levels were not significantly altered, the levels of p-ERK1/2 and p-AKT Ser473 in sorafenib-treated tumours were lower than those observed in vehicle-treated tumours. These findings are in contrast to our previous observation that sorafenib induces paradoxical ERK signalling pathway in gastric carcinoma through upregulation of p-c-Raf Ser338 (Yang et al, 2009). The gene discussed is RAF1; the disease is neoplasm.