GPX4 and hepatocellular carcinoma: A study by Liu et al found that Bufalin functioned as a molecular glue that enhanced E2F2 degradation and inhibited hepatocellular carcinoma growth in vitro and in vivo.[31] Elsewhere, it was observed that Bufalin induced ferroptosis in non‐small cell lung cancer cells by promoting the ubiquitination and degradation of GPX4.[32] In the present study, Bufalin treatment decreased STK33 levels in a time‐ and dose‐dependent manner in TNBC cells.