This immune population showed an increased expression of the activation marker PD-1 both in colitis and dysplasia of Mgat5 KO mice (Figure 3I), suggesting that the controlled tumor growth observed in KO mice is apparently due to the priming of CD8+ T cells alongside γδ T-cell activation that together converge to boost an effective antitumoral immune response with suppression of CAC development. The gene discussed is MGAT5; the disease is dysplasia.