[12] This is similar to the phenotypes of EGFR and ERα knockout mice, which also show absence of ductal growth.

[14][15] Generally, amphiregulin is considered to be a part of type 2 mediated resistance and tolerance, the latter of which occurs by promoting the reestablishment of tissue integrity after damage that is due to acute or chronic inflammation.

[18] Also, in skin derived ILC2s, amphiregulin expression was regulated by the interaction of killer-cell lectin-like receptor G1 (KLRG1) with E-cadherin.

[21] Also, amphiregulin that is expressed from these Tregs can further enhance their function, forming an autocrine positive feedback loop.

[23] Moreover, Tregs that express amphiregulin, along with keratinocyte growth factor (KGF), CD39 and CD73, act on parenchymal cells to promote tissue repair and regeneration.

[25] [26][27] Overexpression of amphiregulin is connected with cancer of the breast, prostate, colon, pancreas, lung, spleen, and bladder.

[28][29][12] It seems that expression of AREG is connected with proliferation of fibroblasts and production of proinflammatory cytokines interleukin 8 and vascular endothelial growth factor (VEGF).

ILC2s are drivers of liver, skin, and pulmonary fibrosis, and their expression of interleukin 13 (IL-13) and amphiregulin is implicated in this process.

Exposure to house dust mite leads to the increase of amphiregulin-expressing pathogenic memory Th2 cells.

The release of them activates the hepatic stellate cells that transform into myofibroblasts, and ultimately promotes liver fibrosis.