In order to stimulate the ACE2/Ang-(1-7)/MasR axis specifically at its most intense site of renal expression, at the proximal tubular brush border, Lores et al. proposed the administration of ACE2 or smaller active ACE2 derivatives (enabling filtration through the glomerular slit diaphragm) under conditions characterized by reduced ACE2 expression and activity, as in diabetic and hypertensive renal disease, and possibly in COVID-19 disease [40]. The gene discussed is ACE2; the disease is hypertensive nephropathy.