In contrast, the SASP’s paracrine effects promote tumor suppression by the activation of either the p53/p21Cip1 or p16INK4a/Rb tumor suppressor pathways; at the same time, the SASP can drive the progression of premalignant cells to develop more aggressive phenotypes through, for example, the stimulation of epithelial-to-mesenchymal transition (EMT) [30]. The gene discussed is CDKN2A; the disease is neoplasm.