Treating cholesterol-addicted BL and GCB-DLBCL cells with HDL NPs activated a compensatory response upregulating de novo cholesterol biosynthesis genes which nearly abolished the expression of GPX4, resulting in ferroptotic death of BL and DLBCL cells in vitro and in vivo, as well in primary samples from patients with different types of lymphoma including DLBCL [19]. This evidence concerns the gene GPX4 and Burkitt lymphoma.