To better understand some of the reasons for the limited response to PD-1 agonists in RA and to uncover novel PD-1 downstream therapeutic targets, we performed a genome-wide CRISPR Cas9 screen using Jurkat T cells stimulated with anti-CD3 and anti-CD28 antibodies with and without recombinant PD-L1. This evidence concerns the gene CD28 and rheumatoid arthritis.