A murine model of Fam13a deficiency exhibited higher numbers of small adipocytes in iWAT, enhanced adipogenic potential, and preserved glucose uptake and insulin responsiveness [33], findings that are very similar to those observed herein in HF-fed LFABP−/− mice, suggesting that Fam13a downregulation may contribute to the hyperplastic iWAT phenotype in these mice. The gene discussed is FAM13A; the disease is hydrops fetalis.