The discovery of amyloidogenic protein domains in the SARS-CoV-2 proteome may be a critical insight. Mutations within amyloidogenic regions can enhance immune evasion and promote viral replication. Monitoring of emerging variants, with a focus on these specific regions, can augment our ability to identify variants of concerns. For example, there is evidence of convergent evolution across SARS-CoV-2 variants in the amyloidogenic region of NSP6 (residues 91-112; https://www.nature.com/articles/s41467-023-36234-4). NSP6 is a transmembrane protein involved in the antagonism of the Type I interferon response. Mutations within the amyloidogenic region (spec. residues 106-108 and 105-107) of the original WA1 variant alters the virus' replication kinetics. The behavior of this mutant mirrors the behavior of the Alpha variant and Omicron sublineages (natural deletion of NSP6 residues 106-108). Mutants are less susceptible to interferon alpha treatment, are more virulent (WA1 mutant outcompetes wildtype) and exacerbate dysregulation of the inflammatory response (cytokine storm).