Single-point mutations have been shown tosignificantly impactfibrillation kinetics and morphologies of sequences involved in pathologiessuch as Alzheimer’s disease and corneal stromal dystrophies.14,63,64 Likewise, insulin was observedto yield distinct fibrillation kinetics and morphologies as a consequenceof a single amino acid substitution.15 Atthe same time, a number of different small-molecule inhibitors ofpeptide fibrillation have been proposed in the past. This evidence concerns the gene INS and stromal corneal dystrophy.