Interestingly, the correlation of TGFB1 and P-SMAD2 is high for inflammation and cirrhosis while the correlation of TGFB1 and P-ERK is high in HCC (Figure 7C and 7D), implying that chronic, high TGFB1 expression in human livers also shifts the dominant downstream pathway from SMAD to ERK, consistent with previous reports in human cell lines that increased transgenic TGFB1 expression induced a shift from canonical (SMAD) to non-canonical pathway (ERK, AKT, etc.)[22]. This evidence concerns the gene AKT1 and hepatocellular carcinoma.