MicroRNAs are well established suppressors of gene expression at the post-transcriptional level, targeting genes through complementary base pairing then repressing gene expression at the levels of both transcript stability and translation. Recent data from our lab and others however indicate the main response of cells to microRNAs are in-fact transcriptional. We hypothesise many of these effects are explained by the direct regulation of transcription factors by microRNAs, and the knock-on effects which then occur as a result of this primary interaction. Although many studies dismiss such responses as “indirect”, these effects are in-fact central to microRNA function, with microRNA : transcription factor co-regulatory loops being an over-represented motif within genetic networks. I present both bioinformatic and preliminary experimental data identifying such interactions that are likely important components of the miR-200 regulatory network – a critical microRNA that controls Epithelial-Mesenchymal Transition during both development and metastasis. It is likely these responses are not unique to miR-200, but rather reflect a more generalised property of microRNA function.