New research led by Cheng, Nan, and Ji uncovers a paradoxical immunological mechanism wherein regulatory T cells (Tregs) boost the pro-inflammatory T helper 17 (Th17) cell population through an intricate cytokine interplay involving transforming growth factor-beta (TGF-β), interleukin-6 (IL-6), and interleukin-2 (IL-2). This discovery challenges the existing dogma surrounding Treg function and may have profound implications for designing next-generation immunotherapies for autoimmune diseases and cancer by modulating cytokine environments to fine-tune immune responses.