Oxidative stress can contribute to the accumulation of DNA damage, which can increase the acquisition of mutations and the activation of signalling pathways, such as extracellular-signal-regulated kinase (ERK), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and phosphatidylinositol 3-kinase/protein kinase B (PI3/AKT) and reactive oxygen species (ROS)-associated epithelial–mesenchymal transition (EMT), thus promoting tumour development in several cancers including that of the breast, stomach and liver [28,30,36,37,38]. Here, AKT1 is linked to neoplasm.