Ferrostatin‐1 and Z‐VAD‐KFM partially attenuated the GV‐induced growth inhibition, whereas GV regulated ferroptosis and apoptosis through the Hep27‐MDM2‐p53 signaling cascade.[65] On the other hand, lncRNA‐HEPFAL expression was decreased in HCC tissues, and overexpression of lnc‐HEPFAL enhanced ferroptosis by increasing ROS and iron levels, improving ubiquitin‐mediated degradation of SLC7A11, thus increasing susceptibility to erastin‐induced ferroptosis.[66] CPLX2 expression was increased in HCC and predicted poor prognosis in patients with HCC. This evidence concerns the gene TP53 and hepatocellular carcinoma.