They identified Ctnnb1 mutation (S33A) in one out of five tumors, which indicated that in their models, deficiency of Arid1a could cooperate with different oncogene activation, including Ctnnb1 and tumor suppressor gene inactivation to promote tumor formation.[13] In contrast, in our mouse models, AAI induces a high Ctnnb1 mutation rate (9 out of 11) in liver tumor tissues from Arid1aLKO mice with AAI‐specific mutational signature, which resulted in exon 3 skipping of Ctnnb1. The gene discussed is ARID1A; the disease is neoplasm.