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A key factor in the successful infection of a mammalian host by <i>Leishmania</i> parasites is their conversion from extracellular motile promastigotes into intracellular amastigotes. We discuss the physical and chemical triggers that induce this conversion and the accompanying changes at the molecular level crucial for the survival of these intracellular parasites. Special emphasis is given to the reliance of these trypanosomatids on the post-transcriptional regulation of gene expression but also to the role played by protein kinases, chaperone proteins and proteolytic enzymes. Lastly, we offer a model to integrate the transduction of different stress signals for the induction of stage conversion.