To identify candidate susceptibility genes for the CIA small-effect QTL, we compared the list of strain-specific differentially expressed genes with the list of disease-specific differentially expressed genes; 117 genes were shared by both lists (Additional file 3). Figure 3 visualises positions of the 117 genes retrieved from Ensembl [30] in relation to the 8 small-effect QTL. The eight loci were located on 7 chromosomes, 5, 6, 7, 10, 11, 16 and 17. Since the confidence intervals of QTL in F2 progeny are around 20 cM [26], we used 40 Mb as the confidence intervals for all loci. Twenty-one genes were located in the confidence intervals of six of the eight QTL. We located 5, 4, 2, 1, 3 and 6 potential candidate genes within the confidence intervals of loci 1, 2, 3, 5, 6 and 8, respectively, while no candidate gene was identified for loci 4 and 7. Table 3 summarises the 21 candidate genes identified in this study. Two genes, hspa1a and Oas1a, were upregulated at the OA phase of CIA and Oas1a was also upregulated at the PI phase. Except for these two genes, all other 19 genes were downregulated at the chronic phase of CIA. All genes, except hspa1a, showed expression differences between the two strains at the NC phase. Five genes were differentially expressed at all phases of CIA, including H2-Q10, Mapk14, Pscd1, Kpnb1 and Wdr1. Among these five genes, H2-Q10 had a consistently higher expression in the DBA/1 than the FVB/N strain in all CIA phases, while the other four genes had a higher expression in the DBA/1 strain at the early stages, including NC, PI and OA, but a lower expression at the chronic phase. GO term classification analysis revealed that the functional cluster of protein kinase cascade was significantly enriched in the 21 candidate genes. This functional cluster contained four genes, including Mapk14, Mapk8ip3, Stat5a and Gna12.