To test the latter hypothesis, we crossed our Msh2-Lynch mouse model into a Tap1−/− background, which is deficient for the TAP1 transporter required for antigen loading into MHC-I, and consequently lacks CD8 + T cells.11Tap1−/−Msh2-Lynch mice in SPF conditions did not show intestinal tumor development nor differences in survival or in the percentage of MSH2-deficient crypts after TMZ treatment as compared to TAP1-proficient animals, arguing against immunosurveillance in SPF mice (Figure S1(e,f)). Here, CD8A is linked to intestinal neoplasm.