We identified reprogramming in transcription in Sgo1-CIN mice lungs, leading to (1) decrease in protection by glutathione (GSTM5, glutathione pool), (2) increase in DNA damage possibly with CIN itself and with oxidative stress, (3) activation of Wnt signaling (SFRP4-β catenin-cyclinD, Lif1), (4) decrease in T/B-cell activation and immune surveillance (CD80, CD8, IL-1β, IL-6, INF-1α, CD22, CD24), (5) decrease in NK-cell activation and immune surveillance (calreticulin, Itgad, Klra3, Klra9) and (6) others such as actin cytoskeleton disturbance. This evidence concerns the gene CD80 and cervical squamous intraepithelial neoplasia.