We used an adipocyte‐specific Adipoq‐Cre to drive the deletion of Prmt5 in adipose tissues.[35] In general, the observed phenotypes are somewhat similar to those of adipocyte specific PPARγ or mTOR deletion in terms of lipodystrophy.[36] However, in our Prmt5AKO mice the lipodystrophy phenotype was more specific to WAT, especially eWAT and asWAT. Here, MTOR is linked to lipodystrophy.