However, because (1) we show in Figure 4C that inhibition of the enzymes that can convert AGT to Ang II significantly inhibited the K-Ras–induced upregulation of the angiotensin form(s) detected using this ELISA kit, (2) the major physiological role of Ang III is in the brain, and (3) Ang IV does not bind to the AT1-R and our data show a key role of AT1-R activation in K-Ras–mediated signaling, we believe that Ang II is the major form of angiotensin produced in normal and lung cancer cells after K-Ras expression. The gene discussed is AGT; the disease is lung carcinoma.