MAZ, also known as Myc-associated zinc-finger protein, is a transcription factor belonging to the Myc family. It plays crucial roles in multiple biological processes and is associated with several signaling pathways, such as MAPK, AKT-NF-κB, and Wnt/β-catenin. MAZ is important in normal development and also has implications in cancer development [1,2,3,4]. Genetic models, like gene knockout (KO) mouse models, are valuable for studying its functions.

In KO mouse models, disruption of Maz led to abnormal eye development in mice and humans. Key genes in the Wnt cascade, Sfrp2, Wnt2b and Fzd4, were up-regulated, while the Wnt reporter TCF-Lef1 was down-regulated, indicating its role in the Wnt/β-catenin pathway and ciliary margin patterning [4]. In cancer research, silencing of MAZ decreased tumor proliferation and immune evasion in lung adenocarcinoma via regulating KRAS and its downstream AKT-NF-κB signaling [2]. In thyroid cancer, silencing MAZ affected the expression of BRAF, KRAS and LOC547, and inhibited the activation of MAPK signaling, thus suppressing tumor progression [1].

In conclusion, MAZ is essential for normal eye development through its role in the Wnt/β-catenin pathway. In cancer, it promotes tumorigenesis in various cancers like lung and thyroid cancer by regulating key signaling pathways. The use of KO mouse models has been instrumental in uncovering these functions, contributing to our understanding of normal development and cancer biology, and potentially providing new therapeutic targets for cancer treatment.