Exposure of human lung mucoepidermoid carcinoma cells to DOX has been shown to induce Hsp60 lysine acetylation, impairing the formation of the Hsp60/p53 complex related to cancer progression, and thereby increasing the levels of free p53, which in turn activates the tumor-suppressive cell senescence pathway [232]. The gene discussed is TP53; the disease is pulmonary mucoepidermoid carcinoma.