Such activation paralleled an up-regulation of p53, p21, Gadd45γ, an increased expression of cleaved-caspase 3, an increase in the number of TUNEL-positive (apoptotic) cells in the lesion and in the liver parenchyma, and a down-regulation of PCNA and Cyclin A. Activation of the metabolic pathways which govern growth arrest and apoptosis also paralleled the previously described decrease of lymphocyte proliferation and of cytokine production observed at the late stage of experimental infection [10], [11], [12]. The gene discussed is CCNA2; the disease is infection.