AKT1 and neoplasm: Employing a combination of cellular, biochemical and genetic experiments, we showed that (i) human and murine pericytes express functional Tie2 receptor, (ii) Tie2-silenced pericytes have a pro-migratory phenotype, (iii) Tie2 downstream signalling in pericytes involves Calpain, Akt and FOXO3A, (iv) Ng2-Cre-driven deletion of pericyte-expressed Tie2 delays developmental angiogenesis and vessel maturation, and (v) Tie2 deletion in pericytes results in a pro-angiogenic tumour vasculature with enhanced tumour growth.