CTNNB1 and neoplasm: CTNNB1 exon 3 mutations, such as S37C, are considered to be activating and lead to activation of the Wnt pathway.[15] CTNNB1 mutations have been reported in 19% of HCC.[7] PTPRD, a tumor suppressor, plays an essential role in dephosphorylating STAT3 (Figure 2).[16] Mutations in PTPRD occur only sporadically in HCC (1%).[7] S1845fs*2 is a frameshift mutation that truncates the PTPRD protein within the second tyrosine phosphatase domain (amino acids 1644-1903) only 1 amino acid from the phosphatase active site, possibly resulting in an inactive protein.