The CMAP analysis has been integrated by us into the systems biology tool suite in Nephromine and can be readily employed by the scientific community not only to IgAN but to all glomerular diseases available in Nephromine. The Connectivity Map datasets have been used to predict and prioritize pairs of drugs that Obatoclax reverse or aggravate the direction of differential gene expression. With this approach we identified several compounds predicted to reverse the gene expression changes associated with Pseudoginsenoside-F11 endocapillary proliferation. Resveretrol emerged as a potential novel compound with this potential therapeutic effect, and interestingly in our analysis both methylprednisolone and corticosterone were predicted to reverse the E1 transcriptional responses when used in combination with resveratrol. This compound, a polyphenol naturally occurring in grapes, has been shown to have attenuate kidney injury induced in the ischemia-reperfusion rat model through stimulation of nitric oxide production and moderation of oxidative stress. Most recently, resveratrol has been found to attenuate experimental diabetic nephropathy, related in part to suppression of VEGF and angiopoietin 2 -induced changes in glomerular permeability. The favourable tolerability profile of this compound in humans make this a potential new agent for therapeutic trial. In summary, we have used a novel approach to identify a distinct glomerular molecular signature associated with endocapillary proliferation. Our transcriptional and pathway analyses support the clinical observation that this lesion may be modifiable with use of corticosteroids. We have also identified therapeutic targets and agents for future study in treatment of IgAN.Thus far, only a few studies have revealed unique cardiac transcriptomic signatures associated with HF using deep RNA-Seq. Others have employed RNA-Seq in conjunction with other techniques to obtain a more comprehensive molecular characterization of HF. Despite the emerging data on RNA-Seq, a clear differentiation between the two major causes of HF, ICM and DCM, based on their transcriptome profiles has not been established yet by this approach.