Depletion of PR130 by miR-652 and its epigenetic silencing mediated by histone deacetylases (HDAC’s) -1, 2, and 3 promote cancer cell growth and migration while leading to the accumulation of DNA replicative stress due to loss of PR130-PP2A regulation on ATM, ultimately resulting in sustained suppression of replicative stress-induced checkpoint signaling cascade (129, 132, 133, 134, 135). This evidence concerns the gene PPP2R3A and cancer.