2013; Mohamed et al. 2016; Kitade et al. 2017; Masarone et al. 2018). Besides, independent of oxidative stress, T1DM is associated with several independent pathological mechanisms that stimulate hepatic lipid synthesis steatosis. These include impaired VLDL-c secretion, increased glucose uptake and conversion to fats, abnormally upregulated transcription factors including the carbohydrate-responsive element-binding protein (ChREBP), and the sterol regulatory element-binding protein 1 (SREBP1c) (Bhatt and Smith 2015). The gene discussed is MLXIPL; the disease is steatosis.