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Adaptive change in gene expression is one of the earliest responses of heart to hypertrophy. Gene transcription is tightly regulated by systematic recruitment of factors including positive and negative elongation complexes of RNA Pol II. Recently we embarked on the task of deconstructing the transcriptional machinery in the heart, by examining Pol II and TFIIB dynamics across the genome in sham and hypertrophied hearts. In this study, we continue examining the active transcriptional code by measuring occupancy of two interdependent factors that belong to positive (PTEFb) and negative (NELF) elongation complexes, Cdk9 and NelfA, respectively. Studies in non-cardiac cells have implicated these two factors in the regulation of promoter (prom) clearance of pol II, where Cdk9 mediated phosphorylation of NelfA results in its release from paused pol II and initiation of productive elongation. As expected, we observed increase Cdk9 (>1.5) association with proms in 59.7% of expressed genes (8257 of 13816), while 6% show decrease in prom Cdk9 (