Editing Argument from poor design (section)

==Counterarguments==
===Specific examples===
[[Intelligent design]] proponent [[William Dembski]] questions the first premise of the argument, claiming that "intelligent design" does not need to be optimal.<ref>{{cite book |last=Dembski |first=William |author-link=William Dembski |title=Intelligent design: the bridge between science & theology |publisher=InterVarsity Press |year=1999 |isbn=0-8308-2314-X |page=261}}</ref>

While the [[vermiform appendix|appendix]] has been previously credited with very little function, research has shown that it serves an important role in the fetus and young adults. Endocrine cells appear in the appendix of the human fetus at around the 11th week of development, which produce various biogenic amines and peptide hormones, compounds that assist with various biological control (homeostatic) mechanisms.  In young adults, the appendix has some immune functions.<ref name=SA>{{cite web |first=Loren G. |last=Martin |date=October 21, 1999 |url=http://www.scientificamerican.com/article.cfm?id=what-is-the-function-of-t |title=What is the function of the human appendix? |publisher=[[Scientific American]] |url-status=live |archive-url=https://web.archive.org/web/20121009062840/http://www.scientificamerican.com/article.cfm?id=what-is-the-function-of-t |archive-date=October 9, 2012 }}</ref>

===Responses to counterarguments===
In response to the claim that uses have been found for "junk" DNA, proponents note that the fact that some [[non-coding DNA]] has a purpose does not establish that all non-coding DNA has a purpose, and that the human genome does include [[pseudogenes]] that are nonfunctional "junk", with others noting that some sections of DNA can be randomized, cut, or added to with no apparent effect on the organism in question.<ref>{{cite web |first=Mark |last=Isaak |year=2004 |url=http://www.talkorigins.org/indexcc/CB/CB130.html |title=Claim CB130 |publisher=Talk.Origins |url-status=live |archive-url=https://web.archive.org/web/20060911070043/http://www.talkorigins.org/indexcc/CB/CB130.html |archive-date=2006-09-11 }}</ref> The original study that suggested that the ''Makorin1-p1'' served some purpose<ref>{{cite journal | last1 = Hirotsune | first1 = S | last2 = Yoshida | first2 = N | last3 = Chen | first3 = A | last4 = Garrett | first4 = L | last5 = Sugiyama | first5 = F | last6 = Takahashi | first6 = S | last7 = Yagami | first7 = K | last8 = Wynshaw-Boris | first8 = A | last9 = Yoshiki | first9 = A. | year = 2003 | title = An expressed pseudogene regulates the messenger-RNA stability of its homologous coding gene | journal = Nature | volume = 423 | issue = 6935 | pages = 91–6 | doi = 10.1038/nature01535 | pmid = 12721631 | display-authors = etal | bibcode = 2003Natur.423...91H | s2cid = 4360619 }}</ref> has been disputed.<ref>{{cite journal | last1 = Gray | first1 = TA | last2 = Wilson | first2 = A | last3 = Fortin | first3 = PJ | last4 = Nicholls | first4 = RD | year = 2006 | title = The putatively functional Mkrn1-p1 pseudogene is neither expressed nor imprinted, nor does it regulate its source gene in trans | journal = Proc Natl Acad Sci USA | volume = 103 | issue = 32 | pages = 12039–12044 | doi = 10.1073/pnas.0602216103 | pmid = 16882727 | pmc = 1567693 | bibcode = 2006PNAS..10312039G | doi-access = free }}</ref> However, the original study is still frequently cited in newer studies and articles on pseudogenes previously thought to be nonfunctional.<ref>{{cite web|url=https://scholar.google.com/scholar?oe=utf-8&um=1&ie=UTF-8&lr&cites=16337157008352528383|title=Google Scholar|website=scholar.google.com}}</ref>