Zfp292, also known as ZNF292, is a transcription factor that plays crucial roles in multiple biological processes. It is involved in the regulation of innate lymphoid cell (ILC) development and function, as well as cell-cycle progression [1,2].

In the context of ILCs, deletion of Zfp292 led to abrogation of the maintenance of intestinal group 3 ILCs (ILC3s), making mice susceptible to bacterial infection. This indicates that Zfp292 is essential for ILC3 maintenance [1]. In retinal progenitor cells, Zfp292 was identified as a target of m6A and a potent inhibitor of cell-cycle progression. Conditional deletion of Mettl14, which is involved in m6A methylation, affected the cell-cycle exit of late-born retinal progenitor cells, suggesting an important role of m6A-mediated regulation of Zfp292 in cell-cycle control [2].

In conclusion, Zfp292 is essential for the maintenance of ILC3s, which is important for immunity and resistance to bacterial infections. It also plays a significant role in regulating the cell-cycle progression of retinal progenitor cells. Gene knockout and conditional knockout mouse models have been instrumental in uncovering these functions of Zfp292 in the context of these biological processes and related disease-susceptibility conditions.