Otud7b, also known as Cezanne, is a deubiquitinase that plays crucial roles in multiple biological pathways. It is involved in regulating autophagy-innate immune signaling crosstalk, mTORC2 signaling, Wnt signaling, and is associated with various physiological and pathological processes such as antiviral immunity, cell growth, and cancer development [1,2,3].

In terms of specific findings, genetic deletion of Otud7b in mice suppresses Akt activation and Kras-driven lung tumorigenesis, revealing its role in mTORC2/AKT signaling-related tumorigenesis [2]. In a murine malaria infection model, DC-specific Otud7b-deficiency led to DC apoptosis and failure to induce CD8+ T cell-mediated brain pathology, highlighting its importance in dendritic cell survival during infection [4]. Also, in mouse models of retinal degenerative diseases, Otud7b -/- mice showed increased cone photoreceptor degeneration, indicating its role in protecting cone photoreceptors [5].

In conclusion, Otud7b is a multifunctional deubiquitinase. Through gene knockout (KO) and conditional knockout (CKO) mouse models, its roles in tumorigenesis, immune-related cell survival, and retinal cell protection have been revealed. These findings contribute to understanding the underlying mechanisms of related diseases and may provide potential therapeutic targets.