TRIP4 and neoplasm: For example, DDRGK1 interacts with IκBα and regulates its stability, and its deletion inhibits tumor cell proliferation.[20] Furthermore, by interacting with activating signal cointegrator 1 (ASC1), DDRGK1 regulates ASC1 UFMylation and promotes ER‐positive breast cancer development.[21] However, DDRGK1 has also been shown to maintain p53 stability and impair the growth of colon cancer via cooperation with UFM1 and covalent modification of p53.[22] Without further research, it is difficult to fully characterize the function of DDRGK1 in tumors.