A number of studies have demonstrated that PI3Kδ inhibitors (INK007, IPI-145, CAL-101) possess pronounced translational potential—capable of attenuating migration, invasion, and cytoskeletal remodeling of RA-FLSs by 60–85% under PDGF-BB or TNF-α stimulation, concomitant with blockade of AKT, Rac1, and PAK phosphorylation [23,24]. This evidence concerns the gene RAC1 and rheumatoid arthritis.