Recent study demonstrated that adipose tissue-specific MDM2 haploinsufficiency (Mdm2Adi+/−) driven by Fabp4 promoter-Cre led to a marked increase in body weight, adipose tissue mass, glucose intolerance, and hepatic steatosis in young mice at least in part through promoting nuclear exclusion of the transcriptional cofactors, MORC2 and LIPIN1, and thereby possibly hampered adipocyte function by antagonizing LIPIN1-mediated PPARγ coactivation (Hallenborg et al., 2021). This evidence concerns the gene FABP4 and Glucose intolerance.