Next, we aimed at identifying the origin of the elevated tumor burden observed upon genetic disruption of Cic. To this end, we infected KP as well as KPCic mice with Ad-Cre and quantified clusters of X-Gal+ cells as a surrogate marker for KRASG12V expression 4 weeks post-infection (Guerra et al, 2003; Mainardi et al, 2014). The gene discussed is CIC; the disease is infection.