Objective: To explore whether Atorvastatin (Ator) can induce ferroptosis in pancreatic beta-cell line MIN6 cells and its possible mechanism. Methods: MIN6 cells were divided into normal group, Ator group (25μmol/L), Ator+apoptosis inhibitor (Z-VAD-FMK) group (10μmol/L), Ator+necrostatin-1 (Nec-1) group (10μmol/L) and Ator+ferrostatin-1 (Fer-1) group (5μmol/L). Cell viability was detected by cell counting kit-8 (CCK8) method. The ultrastructure of cells was observed by transmission electron microscopy. The levels of reactive oxygen species (ROS) and Fe2+ were observed by fluorescence microscopy. The contents of malondialdehyde (MDA) and glutathione (GSH) and were detected by enzyme-linked immunosorbent assay (ELISA) method. Real-time quantitative PCR was used to detect the mRNA levels of caspase3, receptor-interacting protein kinase 3 (RIPK3), acyl-CoA synthetase long-chain family member 4 (ACSL4), prostaglandin endoperoxidase synthase 2 (ptgs2) and glutathione peroxidase 4 (GPX4). Western blotting was used to detect the proteins levels of 4-hydroxynonenal (4-HNE) and GPX4. Results: Compared with the Ator group, cell viability of MIN6 was higher in Ator+Z-VAD-FMK group and Ator+Fer-1 group (P<0.01). MIN6 cells, which were treated with Ator to exhibit the characteristic morphologic features, were associated with apoptosis, ferroptosis and autophagy under transmission electron microscopy. Compared with the control group, in Ator group, the levels of the intracellular Fe2+, MDA and ROS were increased and GSH was decreased. The mRNA relative expression levels of caspase3, ACSL4 and ptgs2 were increased, as well as the protein relative expression leve of 4-HNE (all P<0.05). The mRNA and protein relative expression levels of GPX4 was decreased (P<0.05). Compared with the Ator group, in Ator+Fer-1 group, the levels of the intracellular Fe2+, MDA and ROS were decreased and GSH was increased. The mRNA relative expression level of ACSL4 was decreased and GPX4 was increased (all P<0.05). The protein relative expression levels of 4-HNE was decreased and GPX4 was increased, though the changes were not statistically significant. Conclusion: Atorvastatin may induce ferroptosis in MIN6 cells by down-regulating GPX4 expression through inhibiting mevalonate pathway.