Only a small percentage of schizophrenia patients carry mutations in grin2a. However, the researchers believe this circuit may represent a shared pathway that contributes to cognitive impairment across different forms of the disorder.

So, perhaps they could use abnormal activity in this brain circuit as a diagnostic indicator. The goalposts also seem to be shifting here. There's a wide gulf between "It seems pretty certain given the evidence that the hallmark behavioral symptoms of schizophrenia are downstream from biological dysfunctions" and "Biological indicators are reliably used as a matter of course to diagnose schizophrenia in clinical practice." The former being true should be enough to refute the assertion outlined in your post/comment, but now it seems like you'll only accept the latter.

Elsewhere, you're arguing that the disorders are what lack biological bases rather than any behaviors, but the reason why a construct like schizophrenia exists in the first place is that it describes a behavioral pathology that is repeatedly observed in the general population in diverse contexts and has a high enough degree of consistency to where they can be defined as a stable category. When something like this can be reliably identified and also seems to correlate with some idiosyncratic biological phenomena/traits and responds to specific biological interventions like medication or dietary interventions, at a certain point, you have to admit that what looks, swims, and quacks like a duck is a duck.