A lot of this depends upon the particulars of each and every patient. Regardless of whether or not a given biologic is given to target a specific cytokine that is believed to be driving the disease in a given patient, there is no guarantee it will work. From my reading, and discussions with doctors, it looks to be the IL-17/IL-23 axis that is the primary driver of disease, and everything else basically happens downstream. So if you can address PsA at this axis, then theoretically, you can better affect a positive disease outcome for the patient. That being said, there is plenty of evidence to support that concomitant use of traditional DMARDs with bDMARDs may prove more efficacious in limiting immunogenicity in biologic use. Furthermore, it's still not well understood exactly what role each of these cytokines plays throughout the duration of the disease over time; i.e. which cytokine drives skin involvement, which one drives enthesitis, and so forth. And then there are the JAK inhibitors, which is a totally different class of drugs all together. So you could spend a lot of time getting tested for various cytokines, and it may well prove fruitless in your search for an ideal treatment model. So rheumatologists basically prescribe based upon their experience and knowledge of what may work based upon where they believe a patient is in their stage of disease development.