The destruction of disulfide bonds liberates cysteine from cystine as well as homocysteine from homocystine. N-acetyl-cysteine (NAC) is better absorbed than other cysteine or cystine supplements. Aside from its oxidation to cystine, cysteine participates in numerous post-translational modifications. Two crosslinked cysteines form a cystine molecule. The presence of cystine in urine is often indicative of amino acid reabsorption defects. Agouti signalling peptide adopts an inhibitor cystine knot motif. This antiporter imports cystine and exports glutamate, which are both amino acids. Cystinosis is an LSD characterized by the abnormal accumulation of the amino acid cystine. However, in contrast to the other cystine knot proteins, IL-17F lacks the third disulfide bond. This ultimately leads to buildup of cystine in lysosomes, where it crystallizes and damages cells. Cystinosis is usually treated with cysteamine, which is prescribed to decrease intralysosomal cystine accumulation. For example, those with cystinuria, cystinosis, and Fanconi syndrome may form stones composed of cystine. Adequate hydration is the foremost aim of treatment to prevent cystine stones. People with cystine stones should consume 5 to 7 liters a day. Cystine serves as a substrate for the cystine-glutamate antiporter.