In human transcriptome data from subjects with glomerular disease, the glomeruli from APOL1 high-risk subjects, compared to APOL1 low-risk subjects, manifested alterations in glomerular gene expression that were mapped to interferon and NF-kB pathways, both of which lie downstream of activated PKR32 HEK293FT over-expressing cell also needed interferon pre-treatment to induce sufficient PKR protein for PKR activation on the target RNA (Supplementary Figure 7a)23. This evidence concerns the gene NFKB1 and glomerular disorder.