Gaillard et al (1999) reported that sIL-6R has a high affinity for IL-6, and forms a complex with about 70% of secreted IL-6 in the blood, which enhances the biological effect of released IL-6 (Kovacs, 2001). Becker et al (2004) also reported that IL-6 signalling required tumour cell-derived soluble IL-6R rather than IL-6R, and that suppression of TGF-β-dependent IL-6 trans-signaling prevented tumour progression in vivo . The gene discussed is TGFB1; the disease is neoplasm.