CTNNB1 and neoplasm: Studies have shown that the N-terminal domain of CTNNB1 contains S45 and T41 residues, which regulate the stabilization of CTNNB1.[10] In addition, a study has shown that T41A or S45F mutations can weaken immunotherapy by affecting the infiltration of T cells and tumor-associated macrophages in the tumor microenvironment of AF.[10] In this case, the T41A mutation in exon 3 of the CTNNB1 was detected through Sanger sequencing, further confirming the diagnosis of duodenum-derived AF.