CARHSP1 is a cold-shock domain-containing protein that functions as an mRNA stability regulator with multiple roles in metabolism, inflammation, and cell fate. Mechanistically, CARHSP1 binds to mRNA 3'-UTRs—particularly TNF-α mRNA—to enhance their stability and protein expression 1. The protein localizes to cytoplasmic processing bodies and exosomes, with its function regulated by Akt and calcineurin phosphorylation 1. At the transcriptional level, CARHSP1 negatively regulates gluconeogenic genes (G6Pc and PEPCK1) through physical interaction with and inhibition of PPARα activity 2. Clinically, CARHSP1 dysregulation is implicated in multiple disease states. In glioblastoma, elevated CARHSP1 expression drives radioresistance via inflammatory TNF-α signaling activation, and high CARHSP1 levels correlate with poor radiotherapy outcomes 3. In atherosclerosis, CARHSP1 is targeted by miR-155 in a negative feedback loop to suppress TNF-α-mediated inflammation 4. Additionally, low-temperature stimulation decreases CARHSP1 expression, reducing interferon-β production and increasing influenza susceptibility 5. CARHSP1 also participates in pluripotency maintenance as part of OCT4/SOX2/CARHSP1 complexes binding the NANOG promoter in human pluripotent stem cells 6. These findings establish CARHSP1 as a multifunctional regulator linking metabolic, inflammatory, and developmental processes, with potential as a therapeutic target in diabetes, cancer, and viral infection.