Increasing evidence suggests that interactions of amyloidogenic polypeptides with other polypeptides are crucial modulators of amyloid self‐assembly.6 For instance, high‐affinity interactions of non‐fibrillar species of IAPP with insulin or amyloid β peptide (Aβ40(42)) of Alzheimer's disease (AD) have been found to suppress IAPP amyloidogenesis in vitro.6c, 6e, 7 In addition, LL‐37 was recently shown to interact with Aβ42 resulting in suppression of Aβ42 amyloidogenesis and neuroinflammation in vitro.6b This evidence concerns the gene CAMP and Alzheimer disease.