TF and schizophrenia: Importantly, we previously have demonstrated that our EPBD simulations can account for single-nucleotide polymorphisms responsible for non-local binding effects (in noncoding parts of the human genome) associated with schizophrenia [45], and that our simulations can serve to engineer DNA promoter functionality in vitro[39] and in vivo[61], to modify the strength of a TBP binding site (i.e., the TATA-box) in vitro[46], and to predict the YY1 TF binding sites in cells [47].