We next investigated the ability of LTβR signalling to modulate hepatic tumour progression in models driven by only AKT,29 CAT30, 31 or NICD.26 Sequential serum analyses of Guassia Luciferase, AST, ALT and total bilirubin levels suggest that anti-LTβR treatments selectively promote AKT-initiated tumour progression (figure 5A), which was consistent with significantly increased liver weights at day 90 (figure 5B) and survival observed in AKT/anti-LTβR-treated mice (figure 5C). Here, LTBR is linked to neoplasm.