Leong JY, Chen P, Yeo JG, et al. - Investigators examined the circulatory reservoir of CD4⁺ immune subsets at the single-cell resolution with mass cytometry (cytometry by time of flight) of individuals with juvenile idiopathic arthritis (JIA) (n = 20) who revealed continuous clinical inactivity for at least 6 months with anti-TNFα and were afterward withdrawn from therapy for 8 months, and scored as relapse or remission. In relapse individuals, former to therapy withdrawal, an inflammatory memory subset of CD3⁺CD4⁺CD45RA^-TNFα⁺ T cells deficient in immune checkpoints (PD1^-CD152^-) was noted. In disease-centric pathways involving T-cell receptor activation, apoptosis, TNFα, nuclear factor-kappa B and mitogen-activated protein kinase signaling, transcriptomic profiling exhibited the disparity between relapse and remission individuals. Thus, it was discovered that a novel discriminatory immunomic and transcriptomic signature is related to relapse persons and may demonstrate how relapse occurs.