Figure 2.

In response to DNA damage agents, Akt is activated through different mediators, including ATM, ATR, DNA-PK and RNF168. In turn, activated Akt inhibits DNA repair pathways, resulting in genomic instability, such as gene mutation, deletion and recombination. At the same time, Akt blocks the DNA damage stress-induced apoptosis to promote cell survival. As a result, these 2 events allow cells to select for favorable genetic alterations to facilitate tumorigenesis.