Tumor necrosis factor xcexb1 (TNF-xcexb1) is a key regulator of inflammation and rheumatoid arthritis (RA). TNF-xcexb1 blocker therapies can be very effective for a substantial number of patients, but fail to work in one third of patients who show no or minimal response. It is therefore necessary to discover new molecular intervention points involved in TNF-xcexb1 blocker treatment of rheumatoid arthritis patients. We describe a data analysis strategy for predicting gene expression measures that are critical for rheumatoid arthritis using a combination of comprehensive genotyping, whole blood gene expression profiles and the component clinical measures of the arthritis Disease Activity Score 28 (DAS28) score. Two separate network ensembles, each comprised of 1024 networks, were built from molecular measures from subjects before and 14 weeks after treatment with TNF-xcexb1 blocker. The network ensemble built from pre-treated data captures TNF-xcexb1 dependent mechanistic information, while the ensemble built from data collected under TNF-xcexb1 blocker treatment captures TNF-xcexb1 independent mechanisms. In silico simulations of targeted, personalized perturbations of gene expression measures from both network ensembles identify transcripts in three broad categories. Firstly, 22 transcripts are identified to have new roles in modulating the DAS28 score, secondly, there are 6 transcripts that could be alternative targets to TNF-xcexb1 blocker therapies, including CD86--a component of the signaling axis targeted by Abatacept (CTLA4-Ig), and finally, 59 transcripts that are predicted to modulate the count of tender or swollen joints but not sufficiently enough to have a significant impact on DAS28.