Moreover, studies by Fidalgo and us also suggested that PEE inhibited the binding of angiotensin (Ang) IV to Ang II type 1α receptor (AT1R), increased the expression of angiotensin converting enzyme (ACE), Ang II, and AT1R in the serum and kidney, while decreasing the expression of ACE2, AT2R, and Mas receptor (MasR), thereby eliminating the memory consolidation effect of exogenous Ang IV on male offspring aged 3–6 months, and causing kidney and bone dysplasia, as well as adult (24 weeks after birth) nephrotic syndrome and osteoporosis [182–184]. The gene discussed is AGT; the disease is nephrotic syndrome.