Indeed, the results of our study imply that the suboptimal furin-cleavage sequence, likely evolutionarily conserved to favor efficient export of infectious virus by preventing premature membrane fusion in the secretory pathway and cell entry of immature virus into Fc-receptor-expressing cells by ADE [21], [22], [23], [27], [28], might also, by producing an IFN-inducer, contribute to regulate dengue pathogenesis. Here, IFNA1 is linked to dengue disease.