In an early example, the sulfonyl fluoride BAOD-mSF, was designed to covalently modulate transthyretin (TTR) via modification of Lys15 in the thyroxine binding site.66 Interestingly, the latent fluorosulfate BAOD-FS (Fig. 4) also modified Lys15, though hydrolysis of the resulting adduct yielded the lysine-sulfate.67 Irreversible probes kinetically stabilized TTR and prevented the formation of amyloid fibrils that can cause polyneuropathy and cardiomyopathy. The gene discussed is TTR; the disease is cardiomyopathy.