Other common features in HCC pathogenesis are genomic instability and genetic events such as the inactivation/mutation of tumor suppressor p53, the overexpression of β-catenin, and phosphorylated signal transducer and activator of transcription 3 (pSTAT3), phosphorylated extracellular signal-regulated kinase 1/2 (pERK1/2) and spleen tyrosine kinase (S) SYK (S) expression [17,19,20]. Here, SYK is linked to hepatocellular carcinoma.