Skeletal muscle growth after resistance exercise is regulated by signal transduction pathways that sense signals such as 'loading', time, anatomical location and the concentrations of hormones, amino acids, glycogen and AMP. This information is computed by kinases and phosphatases as well as other proteins that convey information mostly by protein modification or localisation change. The endpoints of these signalling pathways are proteins that regulate transcription, translation/protein synthesis, protein breakdown in muscle fibres and the self-renewal and differentiation of stem cells such as satellite cells. A key regulator of the protein synthesis response to exercise is the AMPK-mTOR signalling network. Whilst many signalling mechanisms within the pathway have been identified, the resistance exercise signal(s) and their sensor (s) are poorly defined. mTOR promotes growth and reverses ageing-related muscle deficits but recent animal studies suggest that at least whole animal activation of mTOR shortens life- span. The antagonist of the mTOR pathway is the myostatin-Smad pathway which inhibits muscle growth. Knockout of myostatin increases muscle size and, but only in some species, muscle function. A growth pathway that has so far not been studied in skeletal muscle is the Hippo pathway. The backbone of this pathway comprises of two kinases that inhibit the transcriptional co- factor Yap1 by phosphorylation. The Hippo pathway regulates organ size in drosophila melanogaster and overexpression of a constitutively active hYAP1 S127A construct in the liver increases liver size [asymp]4-fold in mice. We found that all key Hippo genes are expressed in mouse skeletal muscles, C2C12 myoblasts and myotubes and that Yap is a novel regulator of myogenesis. In vivo experiments are now required to test the hypothesis that the Hippo pathway regulates growth in skeletal.