A non‐canonical role for ATG proteins has been also described in a model of experimental autoimmune encephalomyelitis (a CD4+ T‐cell‐mediated mouse model of multiple sclerosis) where targeted knockout of Atg5 or Atg7 in DCs abrogates myelin presentation to myelin‐specific CD4+ T cells, hence preventing the accumulation of autoimmune T cells within the CNS and the consequent CNS damage (Bhattacharya et al, 2014; Keller et al, 2017; Berglund et al, 2020). The gene discussed is CD4; the disease is multiple sclerosis.