Tendons are tough fibrous connective tissue structures that connect muscles to bones and transmit muscle-generated forces to the skeleton. The assembly of tendon fibres has been studied intensively, but what are the molecular mechanisms that underlie tendon development? On p. 1351, Ronen Schweitzer and colleagues reveal that TGFβ signalling is crucial for tendon formation and for tendon progenitor (TNP) maintenance. The researchers find that tendons are missing throughout the body of mouse embryos in which TGFβ signalling is disrupted by mutating the genes that encode two TGFβ isoforms (TGFβ2 and TGFβ3) or the TGFβ type II receptor. Although TNPs form normally in these embryos, they are lost in later development, when the primordia of tendons would usually form. As no cell death accompanies this loss, the researchers suggest that TNPs assume an alternative fate. They also demonstrate that TGFβ is a potent inducer of TNP markers in tissue and organ culture. The source of TGFβ and its function in TNP specification and maintenance in vivo now await further investigation.