PRXL2A (peroxiredoxin like 2A) is a multifunctional redox regulatory protein with antioxidant activity that operates across multiple physiological systems. Primarily, PRXL2A acts as a cellular antioxidant, protecting cells from oxidative stress through regulation of the glutathione redox balance 1. In bone metabolism, PRXL2A inhibits RANKL-induced NF-κB and JUN activation, thereby suppressing osteoclast differentiation and supporting bone mass maintenance 1. The protein also functions as an adipokine secreted during fasting that suppresses hepatic de novo lipogenesis via the PRXL2A-PTAFR-AMPK-SREBP1 signaling axis, linking adipose tissue to liver lipid metabolism 2. Additionally, PRXL2A negatively regulates macrophage-mediated inflammation by suppressing MAPK signaling pathway activation and inflammatory cytokine production 3. Disease relevance includes oral squamous cell carcinoma, where PRXL2A upregulation confers oxidative stress resistance and worse prognosis, regulated by miR-125b 4, and steroid-induced osteonecrosis of the femoral head, where reduced PRXL2A expression under oxidative stress promotes osteoclast differentiation and bone destruction 5. PRXL2A emerges as a potential therapeutic target for metabolic and inflammatory diseases.