Is the Evidence from ERVs Falsifiable?

For those not familiar with the notion of falsifiability, I summarise it here. For those who are familiar with it, skip over this paragraph. From Wikipedia - "The concept is also known by the terms refutable and refutability. The concept was introduced by the philosopher of science Karl Popper. ... He proposed that statements and theories that are not falsifiable are unscientific. Declaring an unfalsifiable theory to be scientific would then be pseudoscience.
Falsifiability - Wikipedia https://en.wikipedia.org/wiki/Falsifiability" Popper formalised this scientific principle, but it was always a central part of science - the ability to demonstrate that, while not proving a notion to be true, at least demonstrating that it can withstand the tests you submit it to. The more potentially falsifying tests that the idea can withstand, the more confidence we gain in its veracity. Contrast this with creation "science", that is forced to shun falsifiability tests because it cannot measure up to them.

So what tests or observations can we make that could potentially falsify the conclusion of common descent that we arrive at by studying ERVs?

#1 must be the observations of the positions (loci) of ERVs in genomes. Taking chimps and humans as example species, if the loci of ERVs was unrelated, comparing the ERV loci of one species with another, then the ERV case would collapse immediately, based, as it is, on the notion that these ERVs are inherited from common ancestors.

One observation that could potentially weaken the common descent conclusion, short of falsifying it, would be observations that retroviruses naturally target specific loci, whether in one species or the other. It this was so, common ancestry would not be required to explain what we observe.

Observations determine that 1) the vast majority of ERVs in both species are observed to be in precisely corresponding loci and 2) endogenous retroviruses do not target specific loci. See  Don't retroviruses target particular locations in the DNA? Doesn't this explain corresponding ERVs?

#2 One of the most compelling aspects of the evidence is that the pattern of common ERVs in what evolutionary science already determined are closely related species is reflected in the number of ERVs that they share in corresponding loci. Closely related species (according to conventional evolutionary science) have more ERVs in common than more distantly related species. The principle of parsimony comes in here - the more independent lines of evidence that converge on a conclusion, the more confidence we can have that that conclusion is correct. A potentially falsifying observation would be that this relationship does not hold. If large numbers of ERVs were found to be in common loci in dogs, cats and, say, gibbons, but not in orangs, gorillas, chimps and humans, it would be very difficult to explain.

There is one known case where an ERV is found in chimps and humans, but not in gorillas. This can be accounted for by a phenomenon known as Incomplete Lineage Sorting (check the link). But it would take a lot more cases like this to cause serious doubt about common descent. 

#3 A third potentially falsifying scenario would be the one that establishes that no ERVs are caused by retroviruses, but have always been in organisms' genomes by 'design". But no such evidenced scenario or rationale has been established for this notion. Indeed, everything we do know about retroviruses and ERVs points to ERVs having been integrated into germline cells by exogenous retroviruses.