Scaling complementary metal oxide semiconductor (CMOS) devices beyond the 45-nm node may require the formation of highly doped ultrashallow junctions less than 7 nm deep with high lateral abruptness. To meet these stringent requirements, it is necessary to have a better understanding of the underlying mechanisms of transient enhanced diffusion (TED) of implanted dopants during postimplantation annealing. It is now well accepted that dopant diffusion is mainly mediated by native defects created in the substrate. Some early experimental studies suggested that arsenic (As) TED could be mediated by both interstitials and vacancies while phosphorus (P) and boron (B) TED would exclusively be mediated by interstitials. While various mobile dopant-defect complexes have been identified by extensive first principles quantum mechanical calculations, their relative contribution to evolution of dopant diffusion profiles has not been clarified yet. In this presentation, we will focus on addressing the relative contribution of various dopant-interstitial complexes to diffusion of corresponding dopants, based on extensive first principles calculations. We have found that BI, B2I and B2I2 play an important role in B diffusion, while AsI, AsI2 and PI and PI2 are important diffusing species for As and P diffusion, respectively. The pathways and barriers for their diffusion and dissociation will be presented. Based on the data, we will discuss how these mobile species determine dopant diffusion profiles.