This talking point is based on a misapprehension about how research in genetics takes place. Scientists look at particular pieces of DNA usually because some type of GWAS has implicated a particular locus in some disease(at least that’s how it’s done in most medical research on heritable human diseases). Meaning that a particular cohort of people with particular symptoms have undergone genetic testing, and a correlation between people with those symptoms and particular stretches of their genome has been shown. This then provides a clue to motivate further research into trying to determine what it is about this implicated DNA locus, that could at least potentially contribute to the symptoms.
There’s nobody around, and there never were, EVER, anyone who said “we shouldn’t bother studying this DNA here because evolution says it’s junk”.
That a particular pieces of DNA might be junk-DNA, which can be inferred by how well it is conserved, would still not tell you anything about whether that DNA is likely to contribute a genetic component to a disease of some sort. There are so many was that even nonfunctional DNA, which normally does not contribute to any selected organismal function (whatever that might be, metabolism, development, or what have you), can still end up interfering with “normal” cellular functions under the right conditions.
That’s nice but the problem here is that junk-DNA isn’t a “do-nothing string of no operations”. Junk-DNA is known to still be biochemically active in the sense that the transcriptional machinery will still reliably recruit and express even completely randomized DNA, though most of the time at a low level. That’s actually one of the reasons why junk-DNA is still worth studying, because it can still end up having some effect that can contribute to disease.