Isolated AMφ in recurrent MAS showed a reprograming from the antiinflammatory phenotype seen after systemic MAS resolution, toward a similar proinflammatory phenotype seen in acute MAS with activation of IFN-γ–induced genes such as CXCL9 and IL12A (Figure 8E); it also showed a decreases in TGFB and HMOX1 (Figure 8E), as well as more pronounced changes in miR-146a and miR-125a-5p (Figure 8F). This evidence concerns the gene TGFB1 and macrophage activation syndrome.