LYZ and amyloidosis: Thus, the discovery of these particular kinetic properties of cysteines only devoted to assume a structural role as disulfides in the native protein, as also recently found for Cys75 in human albumin17, is a completely new finding that opens interesting perspectives for the knowledge of molecular mechanisms underlying the correct protein folding during transit in the Golgi, as well as the molecular extracellular events responsible for misfolding diseases5 with a particular emphasis to lysozyme amyloidosis, rare non-neuropathic forms of hereditary amyloidosis32–35.