He is also interested to find new applications of existing cGMP-elevating drugs, such as Viagra, to treat important human diseases. There he obtained a strong background in transgenic mouse methods and contributed to the development of so-called Tamoxifen-dependent Cre recombinases including CreERT2, which is now widely used for the generation of inducible knockout mice as well as for genetic cell fate mapping in mice. In 2002 the Feil group has published the first cardiomyocyte-specific cGK knockout mouse model and by now has generated a “mouse zoo” with several inducible, tissue-specific and rescue mouse mutants. The in vivo phenotypes of these mouse models combined with analyses at the cellular and molecular level demonstrated that the cGKs are major players of cGMP signalling. Surprisingly, the cGMP-cGK axis turned out to promote the growth of multiple cell types in the context of cardiovascular and neuronal disorders as well as cancer. More recently, the Feil lab has established new Cre/lox-switchable mouse models for real-time imaging of cGMP and, more broadly, tracking the behaviour of any specific cell type in vivo. Using these new technologies, they could show that atherosclerotic plaques contain previously unknown macrophage-like cells that are derived by clonal growth and transdifferentiation of vascular smooth muscle cells. Dr. Feil’s work is supported by the Deutsche Forschungsgemeinschaft (DFG) and others, and it receives considerable attention as reflected by a survey that ranked him on position 14 among the most-cited pharmacologists in Germany, Austria and Switzerland (Laborjournal 7-8/2009, corrected online version). Since 2013, Dr. Feil is speaker of the DFG-funded research centre “cGMP signalling in cell growth and survival” (FOR 2060). Since 2019, he is speaker of the DFG research training group "cGMP: from bedside to bench" (GRK 2381).