That is in fact in sharp contrast to many rodent models of renal fibrosis (such as UUO, diabetic nephropathy, lupus nephritis, or chronic allograft nephropathy) that do not allow discriminating whether reduction of established fibrosis by therapeutics was due to amelioration of the underlying disease or the fibrosis itself [31], and to in vitro studies using cell cultures that often require exogenous profibrotic stimuli, such as TGFβ, to augment fibrogenesis. Here, TGFB1 is linked to lupus nephritis.