Trypanosomatid parasites are phylogenetically very distant from their mammalian host and many parasite-specific biological pathways have been biochemically characterized with potential relevance for anti-parasitic drug development. Well documented examples for this divergence include the parasite cellular and organellar organization [10], cell surface structure [11], physiological and nutritional requirements for growth and development [12], and notably the exotic mechanisms of trypanosomatid gene expression and regulation by poly-cistronic transcription, trans-splicing and differential RNA and protein stability [13]. Despite robust knowledge on these parasite-specific processes, only little or no progress has been made to exploit this wealth of potential drug targets to develop anti-leishmanial strategies.