No change of viral load or clonality was observed in HTLV-1-seropositive RA patients who were treated with a TNF inhibitor [28], and the efficacy of a TNF inhibitor was attenuated in HTLV-1-seropositive RA patients, especially in those who were anti-citrullinated protein antibody-positive [29]. Here, TNF is linked to rheumatoid arthritis.