HCAR1 and neoplasm: According to the report by Zhao et al., the authors confirmed that the lactate species in the tumor microenvironment could upregulate the production of MUFAs in tumor cells via the HCAR1/MCT1‐SREPB1‐SCD1 axis, which was capable of suppressing the lipid peroxidation in hepatocellular carcinoma (HCC) cells and ensuring the survival of HCC cells under ferroptosis induction with erastin or RSL3.[125] In contrast, treating HCC cells with the combination of an MCT1 inhibitor (AZD3965) and RSL3 could efficiently initiate lipid peroxidation and induce ferroptosis both in vitro and in vivo.