A functioning growth hormone (GH)-insulin-like growth factor (IGF)-I axis is ordinarily essential for normal growth. In several physiological and pathophysiological conditions, however, growth without GH has been described. GH-deficient newborns can have a length within the normal range, which suggests that other growth factors dominate longitudinal gain during gestation. Obese children grow at a normal rate despite their low serum GH levels and reduced response to pharmacological stimulation tests. Children with hypopituitarism secondary to craniopharyngioma resection may continue to grow and may even show growth rate acceleration if their weight increases significantly. Several possible mechanisms might underlie the growth stimulation in obese children, such as elevated levels of insulin and reduced levels of IGF binding protein-1. Recently, elevated leptin levels in obese children were found to affect the bone growth center, and it may be that leptin also participates in the growth without GH observed in obesity, especially after craniopharyngioma removal. Sex hormones stimulate growth in children with a normal GH-IGF-I axis. In the absence of GH, the sex hormones stimulate growth through a direct GH-independent effect on the bone growth centers. Leptin, insulin, and sex hormones locally activate the IGF system in the epiphyseal growth plate (EGP). Other, undiscovered hormones and growth factors may harbor the ability to directly influence the growth processes in the EGP.