A powerful stressor effect on the ER using DTT leads to a decrease in SELENOF expression and induction of apoptosis.Mice with SELENOF knockout were viable and fertile, with normal brain morphology and no activation of endoplasmic reticulum (ER) stress. Oxidative stress was elevated in the livers, and prominent nuclear cataracts developed at an early age.The expression of SELENOF mRNA was downregulated in the hippocampus and substantia nigra of a Parkinson’s mouse model. The gene discussed is SELENOF; the disease is Parkinsonism.