Specifically, directed studies of CHIKV nsP3 expression alone or in the context of a replicon or full viral infection have shown G3BP1 and G3BP2 are recruited and sequestered into cytoplasmic foci that are critical for CHIKV replication and stable to arsenite- and cycloheximide-induced stress that normally induce SG formation or dissolution, respectively31–37. The gene discussed is G3BP1; the disease is viral infectious disease.