1. Lyu, Xia, Lamb, Janine A, Chinoy, Hector. . The clinical relevance of WDFY4 in autoimmune diseases in diverse ancestral populations. In Rheumatology (Oxford, England), 63, 3255-3262. doi:10.1093/rheumatology/keae183. https://pubmed.ncbi.nlm.nih.gov/38507703/
2. Li, Yan, Li, Jiangxia, Yuan, Qianqian, Sun, Wenjie, Liu, Qiji. 2021. Deficiency in WDFY4 reduces the number of CD8+ T cells via reactive oxygen species-induced apoptosis. In Molecular immunology, 139, 131-138. doi:10.1016/j.molimm.2021.08.022. https://pubmed.ncbi.nlm.nih.gov/34482201/
3. Huang, Ling, Zhong, Lifan, Cheng, Ruxin, Liang, Huaping, Liao, Zhongkai. 2023. Ferroptosis and WDFY4 as novel targets for immunotherapy of lung adenocarcinoma. In Aging, 15, 9676-9694. doi:10.18632/aging.205042. https://pubmed.ncbi.nlm.nih.gov/37728413/
4. Guo, Li, Zhang, Xueliang, Pu, Weilin, Guo, Qiang, Wang, Jiucun. . WDFY4 polymorphisms in Chinese patients with anti-MDA5 dermatomyositis is associated with rapid progressive interstitial lung disease. In Rheumatology (Oxford, England), 62, 2320-2324. doi:10.1093/rheumatology/kead006. https://pubmed.ncbi.nlm.nih.gov/36637178/
5. Bao, Hanxuan, Zhang, Chen, Peng, Xue, Jia, Jingnan, Yang, Yi. . Lack of WDFY4 leads to impaired immune response and poor cancer prognosis. In FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 38, e70128. doi:10.1096/fj.202302498RRR. https://pubmed.ncbi.nlm.nih.gov/39600074/
6. Khani, Marzieh, Shamshiri, Hosein, Taheri, Hanieh, Nafissi, Shahriar, Elahi, Elahe. 2020. BVVL/ FL: features caused by SLC52A3 mutations; WDFY4 and TNFSF13B may be novel causative genes. In Neurobiology of aging, 99, 102.e1-102.e10. doi:10.1016/j.neurobiolaging.2020.09.021. https://pubmed.ncbi.nlm.nih.gov/33189404/