Additional studies have confirmed the role of ERα in preventing hepatic steatosis by showing that liver-specific knockdown of ERα is sufficient to induce hepatic steatosis through a mechanism that seems to involve the regulation of small heterodimer partner (SHP), a transcription factor important in the regulation of hepatic metabolic processes and in the protection against hepatic inflammation (318, 319). Here, NR0B2 is linked to fatty liver disease.