In addition to the known classic ferroptosis-related mechanisms, researchers have also found preliminary conclusions, including the use of ranolazine as an FAO inhibitor to promote ferroptosis (Sekine et al., 2022) and the regulation of low-density lipoprotein receptor-mediated PI3K/AKT pathway to promote ferroptosis in DLBCL tumor cells by progesterone and progestin receptor 3 (Song et al., 2023). The gene discussed is LDLR; the disease is neoplasm.