Analysis of Cd28−/− and Carmil2−/− mouse cohorts showed that both CD28 and CARMIL2 molecules were essential for antitumor rejection since their absence permitted BRAFV600EPtgs−/− tumor growth, whereas Carmil2QE mice rejected the BRAFV600EPtgs−/− tumor as efficiently as WT mice. The gene discussed is CARMIL2; the disease is neoplasm.