MCM2 together with five other proteins forms an abundant protein complex with a well established role in DNA replication. At the same time, MCM2 has been implicated in transcription too. Recently an interaction between MCM2 and EAP30, a component of RNA polymerase II elongation factors, was established. EAP30 is part of the Holo-ELL complex and is known to interact with ELL, another elongation factor, and reverse the inhibitory effect of ELL on transcription initiation. ELL has a direct role in leukemogenesis and also interacts directly with RNA Polymerase II. In this thesis, I investigate the interactions between MCM2 and EAP30 and how it is influenced by ELL. I show that MCM2-EAP30 interaction can be over-ridden by ELL and EAP30-ELL interaction can be precluded by the presence of MCM2. I propose a model in which the abundance of MCM2 can modulate the gene expression patterns regulated by ELL.