Ddit4, also known as REDD1, is a gene that plays a crucial role in regulating the cellular energy hub mTORC1. It suppresses mTORC1 initially and then licenses its re-activation, which is important for normal cell proliferation. The mTORC1 pathway is closely associated with various cellular processes such as growth, metabolism, and autophagy [1,2,3].

In mice, Ddit4-deficient models have provided key insights. Paligenotic Ddit4 -/- chief cells in the stomach maintain constitutively high mTORC1. This leads to increased mitosis of metaplastic cells despite DNA damage, increasing the risk of tumorigenesis. MNU-treated Ddit4 -/- mice had increased spontaneous tumorigenesis after multiple rounds of paligenosis induced by TAM [1].

In conclusion, Ddit4 is essential in regulating mTORC1-related cell proliferation. Gene-knockout mouse models, like the Ddit4 -/- mice, have revealed its significance in preventing the proliferation of damaged cells and thus reducing tumor formation in the context of injury-induced metaplasia in the stomach [1].