The potential of PBMC to express IL-6 and TNF-α increased along with disease progression 6, suggesting a compensatory role for these cytokines in response to progressive fibrosis and accumulation of profibrotic cytokines, TGF-β, angiotensin II, etc. According to Okamoto et al, compensatory increase in IL-6 expression is in favor of naïve T-cells to maturate into Th17 subtype rather than Treg phenotype, counteracting profibrotic function in advanced stages of CHF 10. This evidence concerns the gene TGFB1 and congestive heart failure.