Given the number of CD206 + macrophages, but not CD163+, CD68+, CD86+ or iNOS+ macrophages, was markedly decreased upon microcystin-LR treatment, it was reasonable to assume that microcystin-LR could meliorate pulmonary fibrosis mainly by suppressing CD206+ M2a-like macrophage differentiation. The gene discussed is CD86; the disease is pulmonary fibrosis.