Although Axin1 is known to suppress tumorigenesis by promoting β-catenin proteasomal degradation, several studies have shown that the tumor suppressor function of Axin1 can be independent of β-catenin and that silencing of Axin1 does not lead to the induction of the well-known β-catenin transcription target GS (33, 34). The gene discussed is APC; the disease is neoplasm.