Because two signaling pathways are known to modulate the profibrotic effects of MBG, a question arises whether the profibrotic effect of MBG may be initiated via SMAD-dependent TGFβ1 signaling, which was not the case for preeclampsia and CKD, where a key mechanism is Fli1 dependent [8,10,29]. The gene discussed is TGFB1; the disease is chronic kidney disease.