Thus, lipotoxicity induced by polyunsaturated fatty acid (PUFA) overload results in increased rates of lipid peroxidation (LPO) ultimately leading to the newly discovered type of cell death, ferroptosis. Ferroptosis is a form of regulated necrotic cell death occurring upon accumulation of oxidized lipids causing (plasma) membrane damage and rupture. In contrast to other types of regulated necrosis (pyroptosis and necroptosis) where membrane pore formation is mediated by protein aggregates, ferroptosis membrane rapture seems to occur via propagating LPO. In this respect, ferroptosis can be seen as a failure of LQC to control the level of oxidized lipids and their precursors (e.g., PUFAs), and this eventually directs cells towards elimination. Using combination of cell biology, biochemistry and (epi)lipidomics technologies, we are aiming to elucidate underlying mechanism of LQC against cellular and organismal lipotoxicity.