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The gut microbiota is intricately linked with immune cell maturation and function. Antigen-presenting myeloid cells in the gut lamina propria can capture live microorganisms and microbial antigens and migrate to the mesenteric lymph nodes (mLNs), where they prime naive CD4 T cells. However, this process is disrupted in mice deficient in vitamin A, and it has been previously shown that gut microorganisms drive the production of serum amyloid A proteins (SAAs) in intestinal epithelial cells that facilitate the transfer of vitamin A-derived retinoid to intestinal myeloid cells. Now, a preprint from the same group (not peer reviewed) mechanistically dissects the interplay between the gut microbiota and SAAs in regulating retinoid transfer, myeloid cell migration to the mLNs and subsequent CD4 T cell maturation and gut homing.