In addition, other authors have shown that HG-PTCs-EVs activate downstream molecular targets including constituents of the TGF-β, mTOR, ERK and endoplasmic reticulum stress pathways on naïve PTCs in vitro [71], suggesting that pharmacological interventions to inhibit the shedding of EVs from PTCs might serve as an effective strategy for preventing the progression of DKD [71]. The gene discussed is MTOR; the disease is diabetic kidney disease.