Since these pathways have also been associated with FAP+IL11+ FB in the LP (Friedrich et al., 2021; Ke et al., 2024; Kong et al., 2023; Zhang et al., 2024) and with FAP+ FB that accumulate in rheumatoid arthritis and tumor microenvironments (Croft et al., 2019; Gao et al., 2024), we hypothesize that such changes in TRC are, at least in part, a general response of FB to chronic inflammation. The gene discussed is FAP; the disease is neoplasm.