Collectively, these results suggest that pre-treatment with tRA potentiate pristane-induced immunogenic changes through transcriptional regulation of multiple genes (e.g., Epas1, Arl4c, Alcam, S1pr1) involved in cDC activation and migration, which have been shown to greatly contribute to the pathogenic role of cDCs in glomerulonephritis (61–63). The gene discussed is ARL4C; the disease is glomerulonephritis.