The observed suppression in recruitment, mobbing, differentiation and functional status of MPCs are mediated through Akt/STAT/MAP-kinase mechanisms as a reflection of chronic oxidative stress and probably, enhanced catabolic state in CHF.32-34 It is possible to address to new investigations whether relationships between SUA and proangiogenic MPCs are multidimensional, or if they can be associated with clinical outcomes. The gene discussed is SOAT1; the disease is congestive heart failure.