Kim et al. [32] demonstrated that in patients with RHD, the dysregulation of the immune response of peripheral blood mononuclear cells (PBMC) to GAS resulted in the enhanced production of CD4 T cell-derived proinflammatory cytokines (e.g., granulocyte-macrophage colony-stimulating factor (GM-CSF)) which was accompanied by chronically increased IL-1β. The gene discussed is CSF2; the disease is rheumatic heart disease.