Co‐administration of a BCL‐2 inhibitor and a Bruton's tyrosine kinase (BTK) inhibitor downregulates BCL‐2 protein, upregulates cleaved caspase 3, depletes residual GSH levels and suppresses HMOX1, Nrf2 and GPX4 genes, contributing to apoptosis and ferroptosis in DLBCL cells, particularly in DHL cells [131]. The gene discussed is BCL2; the disease is diffuse large B-cell lymphoma.