Lats1 and Lats2 play a redundant role in maintaining AT homeostasis as revealed by that single knock-out of Lats1 (L1-AKO) or Lats2 (L2-AKO) does not lead to fat loss or induce AT fibrosis (Supplementary Fig. 3o–q), which is consistent with what was reported in other tissues24,25. The gene discussed is LATS1; the disease is ataxia telangiectasia.