Downstream ER stress activates lipolytic cascade in adipose tissue which triggers inflammatory response with increased oxidative stress and production of inflammatory mediators, a process that is likely to contribute to the pathogenesis of autoimmune disorders, associated with CLEC16A. We additionally demonstrate that a pan-JAK/STAT inhibitor drug had a multifaceted effect and partially rescued the lipodystrophy and inflammatory phenotype by modulating ER stress. The gene discussed is CLEC16A; the disease is lipodystrophy.