Ei24, also known as Etoposide-induced protein 2.4 (EI24), PIG8 (p53-induced gene 8), is an endoplasmic reticulum (ER) transmembrane protein. It is involved in multiple essential biological functions, including cell adaptation to ER stress, autophagy regulation, and is associated with pathways such as the unfolded protein response (UPR), calcium signaling, and autophagy-related processes. It plays a crucial role in maintaining cell homeostasis and is implicated in various disease-related processes, making genetic models valuable for its study [1,2].

In gene knockout studies, EI24 knockout in cells causes failure of ER stress adaptation and apoptosis, highlighting its role as a novel anti-apoptotic factor in ER stress signaling [1]. Specific ablation of EI24 in neuronal, liver, and pancreatic β cells leads to deficiency of autophagy flux, indicating its importance in the autophagy process [2]. In addition, in vivo overexpression of EI24 in mouse models of renal interstitial fibrosis, pulmonary fibrosis, and esophageal squamous cell carcinoma shows its inhibitory effects on fibrosis and tumor-related processes, such as epithelial-mesenchymal transition, fibroblast activation, cell proliferation, and drug resistance [3,4,5].

In conclusion, Ei24 is essential for cell adaptation to ER stress and regulation of autophagy. The use of KO/CKO mouse models has revealed its significant contributions in disease areas like fibrosis and cancer, providing insights into potential therapeutic targets. Understanding Ei24's functions helps to elucidate the underlying mechanisms of these diseases and may offer new strategies for treatment [1-4,8].