Although there is no direct evidence that H2S modulates macrophage phenotype in heart failure, Kolluru et al. (2015) using femoral artery ligation model has demonstrated that CSE dysregulation or deficiency as well as endogenous H2S production have a significant effect on monocytes/macrophage recruitment and subsequent expression of angiogenetic factors (bFGF and VEGF) under ischemic conditions. The gene discussed is VEGFA; the disease is heart failure.