This editorial refers to ‘IL-9 aggravates the development of atherosclerosis in ApoE−/− mice’ by W. Zhang et al. , pp. 453–464. Atherosclerosis is a chronic inflammatory disease of the arterial wall driven by innate and adaptive immunity. Atherosclerotic lesions contain a variety of cells including smooth muscle cells, macrophages, and T lymphocytes, as well as other inflammatory cells, such as mast cells and NKT cells. This collection of cells promotes the development of atherosclerosis through the production of inflammatory factors. Among CD4+T cells, Th 1 cells have been shown to exert proatherogenic effects, whereas regulatory T cells (Treg) display atheroprotective properties and the role of Th2 and Th17 cells remains unclear.1 The differentiation of Th cells into effector subsets that secrete specific pro- or anti-inflammatory cytokines is critical for the initiation and progression of atherosclerosis. The development of Th subpopulations is dependent on the expression of lineage-specific transcription factors that are regulated by specific cell–cell interactions, as well as by the cytokine environment. Among these is the recently described Th9 cell subset that preferentially secretes IL-9.2 IL-9 is a pleiotropic cytokine that is highly expressed in diseases where Th2 cytokines, including IL-4, IL-5, and IL-13, are up-regulated, which explains why it was initially considered as a Th2 cytokine. In addition to Th9 or Th2 cells, mast cells, eosinophils, innate lymphoid cells (ILCs), and NKT cells have been shown to be sources for this cytokine.3 The differentiation of Th9 cells is dependent on transcription factors that include PU.1, downstream of …