Zfp292, also known as ZNF292, is a gene with important functions in various biological processes. It is a transcription factor that has been implicated in regulating cell-cycle progression, cell proliferation, and cell-type maintenance. These functions suggest its involvement in key biological pathways related to development, immunity, and potentially cancer [2,3]. Genetic models, such as gene knockout (KO) and conditional knockout (CKO) mouse models, are valuable tools for studying Zfp292's functions.

In the context of innate lymphoid cells (ILCs), deletion of Zfp292 in the hematopoietic system led to a reduction in the number and effector functions of intestinal group 3 ILCs (ILC3s), demonstrating its importance in ILC3 maintenance [1]. In the study of cell-cycle regulation in late-born retinal progenitor cells (RPCs), Zfp292 was identified as a target of m6A and a potent inhibitor of RPC cell-cycle progression. Conditional deletion of Mettl14, which affects m6A deposition, had an impact on Zfp292-related cell-cycle regulation [2]. Also, in the research on gastrointestinal tract tumor progression, ZNF292 was identified as a new human colorectal cancer (CRC) tumor-suppressor gene, suggesting its role in cancer-related processes [3].

In conclusion, Zfp292 plays essential roles in cell-cycle regulation, ILC3 maintenance, and potentially in tumor suppression. The use of KO/CKO mouse models has been crucial in revealing its functions in ILC-related immunity and CRC development. These findings enhance our understanding of the biological processes and disease mechanisms associated with Zfp292, potentially paving the way for new therapeutic strategies in immunological and cancer-related diseases.