AKT1 and neoplasm: To further understand the molecular mechanisms behind the reduction of cell proliferation triggered by mTORC2 inhibition, we analyzed AKT phosphorylation on ser-473, which represents the main target of mTORC2, and ERK1/2 phosphorylation on threonine 202/tyrosine 204 because this kinase is frequently phosphorylated in tumor cells when pro-survival stimuli decrease (Mendoza et al., 2011).