Recent evidence suggested an important role of metallothionein-1G (MT-1G) as a negative regulator of ferroptosis whose genetic and pharmacological inhibition enhance sorafenib anticancer activity both in vitro and in tumor xenograft models leading to GSH depletion and lipid peroxidation without altering iron cellular content (Sun et al., 2016a). The gene discussed is MT1G; the disease is neoplasm.