Moreover, deletion or inactivation of the UBA1-STUB1 axis can stabilize JAK1, a key component of the IFN pathway, enhance IFN signaling, and upregulate the expression of important immune regulatory factors such as CXCL9, CXCL10, and MHC class I molecules, thereby enhancing anti-tumor immune response and effectively alleviating the limitation of ICIs resistance [188]. The gene discussed is IFNA1; the disease is neoplasm.