Our data that a long-term breakdown of mitochondrial architecture and inflammation control in macrophages following prolonged disturbance of CMPK2 expression levels and the established importance of increased inflammation in activated macrophages lend credence to our hypothesis that CMPK2 is an important component of the cellular inflammation rheostat controlling macrophage metabolic and transcriptional response to infections. This evidence concerns the gene CMPK2 and infection.