FAM129B, also known as MINERVA, is a protein that has been implicated in various cellular processes including cell protection, antioxidative responses, and regulation of adipogenesis. It has gained attention for its potential roles in cancer progression and as a therapeutic target. Research indicates that FAM129B can protect cardiomyocytes from hypoxia/reoxygenation-induced injury by inhibiting apoptosis, oxidative stress, and inflammatory response through the enhancement of Nrf2/ARE activation. FAM129B has been identified as an antioxidative protein that can reduce chemosensitivity by competing with Nrf2 for Keap1 binding, which influences the Nrf2/antioxidative response and is associated with poor prognosis in breast and lung cancer. FAM129B plays a crucial role during the early stages of adipocyte differentiation. It is expressed downstream of early genes such as Cebpb, Klf4, Klf5, and Srebf1a, but upstream of Pparg2, indicating its role in the regulation of adipose differentiation. FAM129B has been shown to promote tumor invasion and proliferation in non-small cell lung cancer by facilitating the phosphorylation of FAK signaling, which is associated with adverse clinical outcomes. FAM129B activates Ras, which promotes aerobic glycolysis, a process often observed in cancer cells, and this activation is important for cell cycle progression, tumor cell proliferation, and brain tumorigenesis.