Hence, focusing within the setting of prostate cancer, we sought to investigate whether, like PRK1, PRK2 and PRK3 might also associate with TPα and/or TPβ to mediate TXA2-induced chromatin remodelling and cell growth/metastasis, thereby gaining a greater mechanistic insight into how the TXA2-TP signalling axis, and target of Aspirin, can contribute to prostate tumorigenesis. The gene discussed is PLAT; the disease is medical procedure.