Summary of anti-TNF impact on T cells in RA and possible topics of interest for future investigations. Targets of antitumor necrosis factor (TNF) presented in this figure are developed in the main text. Questions raised, and possible topics of future research, are indicated: What is the mechanism of the increase of transmembrane (tm)TNF expression on macrophages that leads to expansion of inducible regulatory T cells (iTregs)? Are T helper (Th)17 cells definitely not responsible for paradoxical psoriasis? What is the role of interleukin (IL)-17/IL-10 producing T cells in the control of rheumatoid arthritis (RA)? Are anti-TNFs other than ETA modifying maturation of thymus and SLO? Are anti-TNFs modifying T-cell metabolism? Are anti-TNFs modifying T-cell diapedesis? What are the molecular mechanisms of reverse signaling? Is there a significant role for in-vivo reverse signaling? Is PD-1 a therapeutic target in RA? Do T peripheral helper (Tph) cells have specific migratory properties? Are plasmablasts induced by Tph pathogenic? Do they produce anti-CCP antibodies? How to modulate immunization against anti-TNF? How to improve targeted anti-TNF biotherapy?