Specifically, our results show that human patient-derived CMT1A fibroblasts exhibit heightened susceptibility to ferroptosis induction as compared with age-matched healthy control cells, and show indicators of increased ferroptotic stress at baseline, as measured by a reduction in GPX4 levels and elevated lipid peroxides (Figure 2, Figure 3, Figure 4, Figure 5 and Figure 6). The gene discussed is GPX4; the disease is Charcot-Marie-Tooth disease type 1A.