AKT1 and neoplasm: In accord with the results obtained from analysis of mRNA expression, the activation status of AKT and of ERK1/2 (analyzed by the expression of their phosphorylation on Ser 473 and on Thr 202/Tyr 204, respectively) was comparable in tumor lysates extracted from WT, stathmin heterozygous and KO mice (Figure 6C).Overall, our data demonstrated that reducing or ablating stathmin expression did not affect the number of tumors nor their latency nor the molecular alterations typical of the DMBA/TPA-induced carcinogenesis.