This example of citation kiting, along with the others, leaves us with more evidence that FCH is a target for “FH” sales. What is cited as “phenotypic FH” in Sturm et al (below left) is clearly FCH in the source, Ellis et al (top, right). And in Sturm (left) there is no mention of FCH … at all … even though their citation clearly calls for it: the title of the source material itself tells us that FCH can mimic FH. Also note that originally “FH” was defined by the presence of the LDLR mutation. Then due to citation kiting from 2011 on, “FH” included other non-receptor mutations because they were in the receptor “pathway,” i.e., the APOB and PCSK9. Now lipoprotein(a) is not even associated with the receptor pathway and yet is here said to be a “possible cause of clinical familial hypercholesterolemia.” Many of the authors receive pharma money.This is another example of using citation kiting to bring other diseases within the range of “FH” drug sales, and again fitting the pattern that profits Big Pharma: citation kiting results in the assumption that the FCH are FH.