After discontinuation of IFN, clinical and laboratory findings showed resolution of FSGS.[11] Markowitz et al reported a cohort of 11 patients treated with all types of IFN (α, β, and γ) that developed FSGS; these included 3 women who had MS, 2 of whom had comorbid hypertension, and 2 also had coexisting diabetes and obesity.[17] These 3 patients were treated with IFN beta and had varying clinical presentations, including edema, proteinuria, and renal insufficiency.[37] Of note, 1 patient was treated with IFN-β-1a for 4 years and developed proteinuria and renal insufficiency. The gene discussed is IFNA1; the disease is obesity disorder.