UBE2E2 and type 2 diabetes mellitus: When coupled with human GWAS demonstrating associations between SNVs at the UBE2E2 locus T2D and with visceral — as opposed to s.c. — adiposity, we formulated the hypothesis that UBE2E2 loss of function drives negative metabolic sequelae by impairing adipogenesis and healthy adipose tissue development in metabolically protective s.c. depots — i.e., that UBE2E2 loss of function would lead to a phenotype on the lipodystrophic spectrum.