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Unsurprisingly, abundant data demonstrate that MBR mutations promote the accumulation of immature metal‐deficient SOD1 metalloforms, with mutant proteins frequently isolated from expression systems containing little to no bound metals (Table 2).[ 96a , 97a , 98a ] Whilst MBR mutations dramatically impair holo‐SOD1 formation and stability, most are of little consequence to apo‐SOD1 stability, with some mutant apo proteins (H46R, D124V) even exhibiting increased thermodynamic stability relative to wild‐type apo‐protein (Table 2)