Moreover, earlier reports identified CD11b+ inflammatory cells (presumably macrophages) as resources of the major profibrotic agent TGFβ in human biopsies from HF with preserved ejection fraction (HFpEF) patients and attributed this event to the increased collagen I production and ability of biopsy-derived human cardiac fibroblasts to trans-differentiate into myofibroblasts. The gene discussed is TGFB1; the disease is hydrops fetalis.