Since these Mφs are a major source of profibrotic molecules, our results showing increase in TGFβ-1 as well as MMP9 suggest that these Mφs could be contributing both directly and indirectly to fibrotic processes in FH-mediated ICGN through different mechanisms (1,3,8,44). Here, TGFB1 is linked to familial hyperaldosteronism.