Ppp2r2b, encoding protein phosphatase 2 regulatory subunit B, is crucial in multiple biological processes. It is involved in pathways like the mammalian target of rapamycin (mTOR) pathway, and plays a role in the termination of the immune response. Its dysregulation has implications for various diseases, making genetic models valuable for understanding its functions [1,3].

In pancreatic ductal adenocarcinoma (PDAC), HOXC6-induced suppression of Ppp2r2b activates the mTOR pathway, promoting PDAC growth [1]. In bladder cancer, down-regulation of Ppp2r2b promotes cell proliferation, migration, and cisplatin resistance, while restoration of its function enhances cisplatin sensitivity [2]. In systemic autoimmune diseases, inflammation-driven hypermethylation of Ppp2r2b leads to acquired apoptosis deficiency [3]. In spinocerebellar ataxia type 12, bidirectional transcription at the Ppp2r2b gene locus, including the antisense transcript, contributes to pathogenesis [4,5]. In triple-negative breast cancer, Ppp2r2b down-regulation is associated with immune evasion and poor clinical outcomes [6].

In conclusion, Ppp2r2b is essential in regulating multiple biological processes and is implicated in various diseases. Gene-knockout models could potentially further clarify its role in these disease conditions, providing insights into disease mechanisms and potential therapeutic targets for PDAC, bladder cancer, systemic autoimmune diseases, spinocerebellar ataxia type 12, and triple-negative breast cancer.