While efficacy against alternative targets such as eEF2K (NH125) and Semaphorin 5A illustrates the breadth of therapeutic possibilities—manifested by suppressed RA-FLS metabolism and reversible attenuation of inflammation in model systems [28,29]—the paucity of data on biomaterial variability and remission parameters precludes unequivocal conclusions regarding the translatability of these effects. This evidence concerns the gene SEMA5A and rheumatoid arthritis.