As compared with erastin, the target molecules of which are xCT cystine/glutamate antiporter and VADC2/3, artesunate was not specific to mutant RAS-driven cancer cells. For instance, erastin failed to induce cell death of HRAS(G12V)-transfected MEF, although this compound could kill several pancreatic cancer cell lines with mutant KRAS. Furthermore, artesunate-induced cell death occurs even in WT-MEFs and HaCaT without active-mutant RAS. Surely, these phenomena were inhibited by ferroptosis inhibitors such as ferrostatin-1 and DFO, but I wonder why these compounds are lack of specificity in terms of the definition of ferroptosis???