The effect of growth hormone (GH) on various growth processes is generally considered to be indirect, mediated by GH-dependent plasma factors¹—somatomedins—which are produced mainly in the liver^2–4. In vitro, somatomedins stimulate a number of processes^5–10 that apparently are associated with cell growth¹. It has been difficult, however, to induce skeletal growth by the administration of somatomedins in vivo. Daily injections of a partially purified somatomedin preparation failed to induce accumulated longitudinal bone growth using the intravital marker tetracycline or by measuring the nose-to-tail length^11,12. Administration of insulin-like growth factor I (IGF I) which is probably identical to somatomedin C¹³, to hypophysectomized rats has been reported to increase the width of the epiphyseal plate¹⁴. But although this suggests an in vivo effect of IGF I on longitudinal bone growth, such an effect has not been directly demonstrated. Recently, we reported that local administration of human GH (hGH) into the proximal cartilage growth plate of the tibia of hypophysectomized rats stimulated longitudinal bone growth on the side injected with the hormone¹⁵. Further more, we have identified specific binding sites for hGH in cultured chondrocytes from rabbit ear and epiphyses¹⁶. Here, we show that hGH, but not the structurally related polypeptides ovine prolactin or human prolactin, stimulates DNA synthesis in chondrocytes from rabbit ear and from rat rib growth plate, cultured in a chemically defined medium without the addition of serum. Our results suggest that GH directly initiates proliferation in mammalian chondrocytes.