I n tlie present investigation, we have attempted to identify regions of tlie genome in which "obesity genes" potentially reside using robust sib-pair linkage analysis. Data were collected on 1,628 intlivicluals in 301 nuclear families residing in the environs of Qu6bec City during tlie period [1978][1979][1980][1981]. In adtlition to traditional I,lood group antigens and enzyme polyniorpliisms, several phenotypes in tlie obesity domain that are associated with increased morbidity were assessed, including measures relating to heaviness (i.e., the body mass index), body composition and nutrient partitioning (i.e., % body fat), and regional fat distribution without and with stanclarclization for total fat niass (i.e., the sum of six skinfold thicknesses, and the ratio of tlie sums of trunk to extremity skinfold thicknesses). Three consistent patterns of potential linkage relationships with obesity phenotypes were revealed in these data, involving tlie marker loci adenosine deaniinase, tlie Kell blood group antigen, and esterase D, which identify cliromosomal regions 20~113, 7~133, and 13114, respectively. Other potential linkages also were identified in the short a r m of chromosome 1, interesting because of tlie presence of the db and f i t loci on lioniologous regions of chromosome 1 in mouse and rat models of obesity, respectively. Each of the tentative linkage relationships reported here warrant follow-up using alternative nietliods and require replication in intlependent studies.