We observed infection-mimicking conditions induced enrichment of non-stress-related processes within the wos2Δ proteome (i.e., translation, amino acid biosynthesis, and nucleotide metabolism) with decreased responsiveness in major antioxidant enzymes (i.e., Sod1, Cat1, and Cat3), corroborated by an oxidative sensitivity phenotype (i.e., H2O2). The gene discussed is SOD1; the disease is infection.