Yeast cells exposed to hyperosmotic conditions adjust their metabolism in order to increase the production of the compatible solute glycerol. The MAPK Hog1 seems to affect glycerol production rapidly by stimulating flux through glycolysis and long-term via the transcriptional upregulation of genes encoding enzymes in glycerol formation. In addition, the glycerol channel Fps1 rapidly closes after a hyperosmotic shock to ensure efficient glycerol accumulation. Hog1 seems to modulate basal Fps1 activity and the MAPK is needed to allow complete closure of Fps1. Moreover, the expression of a number of metabolic genes is affected in both Hog1-dependent and independent ways. How those changes contribute to osmotic adaptation of yeast cells is not completely understood. To separate and analyze the different roles of Hog1 in the adjustment of metabolism will probably need a time-resolved holistic view on all components involved and a combination of theoretical modelling and experimentation. In addition, there is a need for more detailed analysis of direct and indirect Hog1-targets to elucidate the impact of such regulatory interactions.