With the advent of evidence of local functional RAS system, its implications have been found beyond cardiovascular disorders such that components of classical arm RAS like angiotensin II (Ang II), angiotensin-converting enzyme (ACE), and angiotensin type I receptor (AT1R) are upregulated in synovial tissue of RA specimens and found to be responsible for the exacerbation of RA [7]. The gene discussed is ACE; the disease is cardiovascular disorder.