Deletion of HDAC1 in T cells (using Cd4-Cre; Hdac1fl/fl x Cd4-Cre, designated as HDAC1-cKO) conveys resistance to experimental autoimmune encephalomyelitis (Göschl et al., 2018; Hamminger et al., 2021), collagen-induced arthritis (Göschl et al., 2020), and adoptive T cell transfer colitis (Hamminger et al., 2021), while HDAC1 restrains the pathogenic Th2 cells in allergic airways inflammation (Grausenburger et al., 2010; Khan et al., 2025). Here, HDAC1 is linked to experimental autoimmune encephalomyelitis.