Primarily, this phenotype is activated by IL-4 and IL-13 produced by T helper 2 (Th2) cells,28 and typically identified by their notable expression of functional surface marker such as CD163.29 Nevertheless, macrophage malfunction can hinder the normal tissue repair process and conversely, facilitate the occurrence of fibrosis, the accumulation of type I and III collagen, and the activation of myofibroblasts.30 An excessive amount of M2 macrophages is associated not only with fibrosis, but also with cancer,31 chronic obstructive pulmonary disease (COPD),29 and acute kidney injury.32 The gene discussed is IL13; the disease is chronic obstructive pulmonary disease.