Kim et al. reported that the administration of hydroxychloroquine, a drug used to treat patients with RA, in PBMC-derived human CD4+ T cells inhibits autophagic flux by interfering with mitochondrial superoxide production and induces excessive ROS, thereby inhibiting the proliferation of activated CD4+ T cells (Kim et al., 2021). The gene discussed is CD4; the disease is rheumatoid arthritis.