Fas apoptotic inhibitory molecule 2 (FAIM2), an important member of the transmembrane BAX inhibitor motif containing (TMBIM) family, is involved in multiple biological processes. It has anti-apoptotic functions and is associated with pathways like Wnt/β -catenin [3]. It plays a role in various physiological and pathological conditions, including tumorigenesis, myogenesis, and neuroprotection [3,4,5]. Genetic models, such as knockout (KO) mouse models, are valuable for studying its functions.

In medulloblastoma, FAIM2 expression is decreased in metastatic samples, and its low expression is associated with poor prognosis [1]. In glioma, molecular biology experiments verified a cancer-suppressor role for FAIM2, and it may serve as a potential pan-cancer biomarker for prognosis and immune infiltration [2]. In non-small cell lung cancer, FAIM2 promotes cell growth and bone metastasis by activating the Wnt/β -catenin pathway [3]. In facioscapulohumeral muscular dystrophy, DUX4 via TRIM21 targets FAIM2, leading to cell death and defective myogenesis, and FAIM2 overexpression can rescue the myogenic differentiation defect [4]. In transient brain ischemia, Faim2 up-regulation may contribute to the neuroprotective effects of low-dose erythropoietin [5].

In conclusion, FAIM2 has diverse functions in different biological processes and disease conditions. Model-based research, especially KO mouse models, has revealed its roles in tumor metastasis, prognosis, myogenesis, and neuroprotection. Understanding FAIM2 is crucial for developing potential therapeutic strategies for related diseases.