Until recently, the mechanistic basis for hyperferritinaemia and hyperinflammation in dengue hasn’t been well understood, but recent insights suggest that it occurs due to a combination of unchecked viral replication within macrophages and monocytes, with viral uptake mediated by non-neutralising antibodies from prior infection with a heterotypic dengue serotype, in addition to dysfunctional NK T cells with impaired cytolytic function with reduced perforin and granzyme B production19. The gene discussed is GZMB; the disease is infection.