Although the majority of these studies did not directly look at tumor-associated immune cells or the structure of the extracellular matrix, and post-treatment samples would be complicated by altered proportions of different cell populations, these studies demonstrate that reduction of estrogen activity by both ER degradation and reduced estrogen synthesis has dramatic effects on cytokine/chemokine networks, and components and modifiers of the extracellular matrix and tumor cell responses (such as TGFβ, PDGFRB, and the Hippo pathway) [246,247,248,249]. The gene discussed is PDGFRB; the disease is neoplasm.