We postulated that, since gonadal steroids may affect adiponectin oligomers distribution and circulating leptin levels, partly explaining sex differences in association between inflammatory markers and diabetes risk [23], a dysregulated repertoire of these molecules in prepubertal age would reflect the “quality” of individual adipose cells as well as their association with insulin-resistance better than in adulthood [4], [11], [21], [22], [24], [25], [26]. The gene discussed is LEP; the disease is diabetes mellitus.