We applied parental and IR MCL cells to in vivo xenograft models to validate (1) whether TME stroma promotes tumour progression in both parental and IR MCL cells, (2) whether IR MCL cells conferred greater tumour-forming potential and (3) whether PI3K-AKT-mTOR activation was sustained and β1 was upregulated. The gene discussed is AKT1; the disease is neoplasm.