In regard to the LEPR gene, Clément et al. described a homozygous mutation in the human LEPR gene that resulted in a truncated LEPR lacking both the transmembrane and intracellular domains and, in addition to their early-onset morbid obesity, patients homozygous for this mutation had no pubertal development, with reduced growth hormone and thyrotropin levels, suggesting that leptin is an important physiological regulator of several endocrine functions in humans [90]. Here, LEPR is linked to morbid obesity.