TI - Tumor Phenotype of Transgenic myrAKT Lines . AB - The levels of AKT activation measured as Ser473 PHOSphorylation were functional in all lines , since mammary gland involution was delayed in all transgenic lines (Figure S1) . However , despite genetic ( one or two alleles ) of physiological ( virgin or multiparous ) differences that contribute to different levels of AKT and chimaerism , no differences in the survival of transgenic lines were observed ( Data not shown ) . We did not observe a statistical increase in the number of mammary tumors in any of the transgenic lines . An in deep analysis of the mammary glands of the animals indicated that the transgenic lines showed an increased percentage of intraductal mammary neoplasia ( MIN ) and suckling differentiation ( Figure 2 ) . This increase was observed in all transgenic lines without a clear correspondence with AKT levels or degree of chimaerism , indicating that high levels of AKT are not essential . Only a higher incidence of MIN in almost all transgenic lines is correlated with no pregnancies . A few animals with tumors were also observed , of variable type , with no statistical significance ( Figure 2 ) . The molecular characterization of MIN indicated that MIN from wild type animals were different from to those arising in transgenic mammary glands . Transgenic MIN showed increased AKT phosphorylaTION and were positive for Progesterone receptor ( PR ) , Estrogen Receptor ( ER ) and Estrogen Receptor PHOSphorylation ( ER-P ) (Figure S2) . The few tumors arising from transgenic animals were histologically heterogeneous but could be grouped in two main classes : adenosquamous ( n = 1 ) and carcinomas of different types ( n = 4 ) ( Figure 2 ) . Staining for molecular markers showed that carcinomas presented in general similar molecular pattern ( Figure S2 ) . All of them showed AKT PHOSphorylation and increased levels of ER , ER-P and PR . They also showed strong keratin 6 (CK6) , E-cadherin and p63 staining . Taken together our data indicated that increasing the levels of AKT in the mammary gland was not sufficient to produce a tumoral response in mice . Only a moderate increase in premalignant lesions was observed , and this was independent of the levels of AKT and the degree of chimaerism in the ductal epithelia .