Specifically, the Prmt5‐null adipocytes phenocopy one of the most prominent feature of Seipin‐deficient cells in the formation of “supersized” LDs.[39] Furthermore, Prmt5AKO mice also phenocopy the lipodystrophy and lipidomic profiling phenotypes of the adipose‐specific Seipin KO (ASKO) mice and in vitro behavior of Seipin‐null adipocytes.[25, 40] Consistently, we showed that knockout and pharmacological inhibition of PRMT5 both suppressed Bscl2 expression. The gene discussed is BSCL2; the disease is lipodystrophy.