GPX4 and metabolic dysfunction-associated steatohepatitis: Qi et al. [133] demonstrated that in the MCD-induced NASH model, treatment with the GPX4 activator sodium selenite, the iron chelator desferrioxamine (DFO), and the ferroptosis inhibitor Liproxstatin-1(Lip-1) inhibited the ferroptosis, suppressed inflammatory response, and alleviated NASH, while conversely RSL3 (a ferroptosis inducer) downregulates GPX4 levels and exacerbates the severity of NASH [133].