Thanks Bear!  It was actually the Tian pulication the Rndtbl linked that got me started on my path to investigating the criteria for predicting the characteristics of a 'good' BETi for inflammatory/autoimmune disease.  Those researchers demonstrated that their new BRD4 selective BETis were more effective than RVX-208 at reducing airway inflammation.  BRD4 has been identified as a major target in many of the cancer pathways, possibly because of its ability to interact directly with acetylated lysines on some of the transcription factors involved (IFNgamma, NF-Kbeta) rather than just with acetlyated amino acids on the histones of the associated genes (recall that you noted this in a recent post).  However, the panBETis used in cancer treatment have high toxicities that make them unsuitable for long tretment of inflammatory/autoimmune diseases.  Selective inhibition of BD2s is likely part of the reason the RVX molecules are less toxic.

So...  My current working hypothesis is that a BDR4-selective (and perhaps also somewhat BRDR2-selective), BD2-selective BETi might be the best 'bet' for the design of an inhibitor for auto-immunity/inflammation. 

BTW, the disease that I have an interest in - sarcoidosis - does involve airway inflammation in many cases since it most often is pulmonary.  Both IFNg and NF-Kb are major drivers of the infammation in sarcoidosis and, if it persists, the inflammation leads to fibrosis of the lung (or other affected) tissue - so the recent discussion of the anti-fibrotic properties of BETis was also relevant.

Jupe