FAIM2 (Fas apoptotic inhibitory molecule 2) is an antiapoptotic protein that protects cells from Fas-induced apoptosis through multiple mechanisms. In neurons, FAIM2 directly interacts with the Fas receptor and modulates calcium release at the endoplasmic reticulum through interaction with Bcl-xL, thereby inhibiting caspase-8 activation 1. Beyond its classical antiapoptotic role, FAIM2 functions as a fatty acid synthesis inhibitor in metabolic dysfunction-associated fatty liver disease (MAFLD) by promoting autophagic degradation of CREB-regulated transcription coactivator 2 (CRTC2), with FAIM2 expression decreased in MAFLD patients 2. FAIM2 is implicated in cerebellar development, affecting cerebellar size and Purkinje cell differentiation 1. In disease contexts, low FAIM2 expression correlates with poor prognosis in medulloblastoma metastasis 3 and is involved in neuroprotection against ischemia and bacterial meningitis 1. FAIM2 is also essential for myogenic differentiation; DUX4-induced degradation of FAIM2 via the E3 ligase TRIM21 contributes to facioscapulohumeral muscular dystrophy pathology 4. Additionally, FAIM2 variants are associated with type 2 diabetes and obesity susceptibility in genetic studies 53, suggesting roles in metabolic regulation beyond hepatic lipid metabolism.