In addition to the genetic modification causing the lipodystrophy, nSREBP1c overexpression versus Lmna deficiency, aP2 (i.e., Fabp4) drives Cre expression more broadly than Adipoq, including in adipose tissue macrophages (43), providing one possible reason that the phenotype of aP2-nSREBP1c mice is more extreme than LmnaADKO mice (44). Here, FABP4 is linked to hyperinsulinemic hypoglycemia, familial, 4.