Interestingly, Ftl−/− mice are viable (knock-out of the Fth subunit is embryonic lethal) and do not show signs of neurodegeneration, presence of an inflammatory process, noticeable protein aggregates, or iron accumulation as in patients with HF, suggesting that the deleterious effect(s) caused by mutant FTL subunits in HF are driven by disruption of the ferritin pore structure and unraveling of the C-terminus in the heteropolymer rather than by a loss of normal function of the FTL subunit itself. The gene discussed is FTL; the disease is hydrops fetalis.