Apc, short for Adenomatous Polyposis Coli, is a well-known tumor suppressor gene. It has a crucial role in regulating the Wnt signal transduction pathway and is also an important cytoskeletal protein. The Wnt pathway is fundamental in various biological processes such as cell proliferation, differentiation, and development. Mutations in Apc are strongly associated with colorectal cancer, and it also has links to several neurological disorders [1,2].

Mutations in the Apc gene are responsible for familial adenomatous polyposis (FAP) and play a rate-limiting role in most sporadic colorectal cancers. Loss of Apc function initiates a series of molecular and histological changes following the 'adenoma-carcinoma' sequence. Inactivation of Apc seems to confer both selective advantage for initial clonal expansion and genetic instability for tumor progression, likely through constitutive activation of the Wnt pathway [1]. Apc mutation in colon cancer is associated with a poor response to immunotherapy, characterized by lower tumor mutation burden (TMB), lower expression of immune checkpoint molecules, higher tumor purity, lower MSI-High proportion, and less immune cell infiltration. Gene set enrichment analysis indicates that Apc mutation up-regulates the mismatch repair pathway, which may negatively impact the antitumor immune response [3].

In conclusion, Apc is essential for maintaining normal cellular function, especially in relation to the Wnt signaling pathway and cell-cycle regulation. Its inactivation due to mutations is a key event in the development of colorectal cancer. The study of Apc in gene-knockout (KO) or conditional-knockout (CKO) mouse models, although not explicitly detailed in the given references, would likely further elucidate its role in normal and disease-related biological processes, particularly in colorectal cancer, and potentially aid in the development of new diagnostic and therapeutic strategies.