We previously showed that SSc-ILD monocytes overexpress CXCR4 because of a deficiency in the master signaling molecule caveolin-1 and that this phenotype (that is, low caveolin-1 and high CXCR4) can be generated in normal monocytes by treatment with TGFβ. The gene discussed is CXCR4; the disease is systemic sclerosis.