MAF and rheumatoid arthritis: Aligned with cTfh17 effects we described above, these splenic Tfh17 promote RA manifestation, enhance GC-B responses, and elevate anti-GPI antibody titer (116), supporting the “imprinted” plasticity models, and its adjustment of c-Maf suggests that BCL-6 is not the only factor of tuning Tfh and Th lineage phenotype, and considering c-Maf being the key of GC-Tfh2 generation, supporting the imprinted plasticity model applied to GC-Tfh, where c-Maf is an important participant, as a supplement to its de novo plasticity model (5) supported by evidences in 2.1.2 and 2.1.3.