This shows that the expressions of CTGF, COL1A2 and COL3A1 in response to the perturbation of the silica are more unstable than that of SPARC and TIMP3. Differential regulations of CTGF, COL1A2 and COL3A1 in response to the perturbation of silica between the normal and SSc fibroblasts may imply that the interactions of these three genes with the silica may be involved in the pathogenesis of the SSc. Here, CCN2 is linked to systemic sclerosis.