However, inactivating EBNA3A and EBNA3C simultaneously leads to a very robust activation of p18INK4c expression during the first 3 weeks after infection, confirming EBNA3A/EBNA3C-mediated regulation of CDKN2C. Analysis of control housekeeping genes (e.g., ALAS1) showed no change in the mRNA level (S1A–S1C Fig), but similar analysis of p16INK4a mRNA confirmed what has been widely reported previously [38–40]; that is, inactivating EBNA3C or, to a lesser extent, EBNA3A leads to increased p16INK4a expression. The gene discussed is ALAS1; the disease is infection.