Our previous report pointed out that VPA could disrupt HR and NHEJ through targeting the activity of BRCA1, Rad51, and Ku80 [7], may enhance radiation-induced apoptosis and serve as a radiosensitizer in a p53-dependent manner in colorectal cancer cells [26], and downregulate both protein expression and foci accumulation of BRCA1 and RAD51 in LNCaP and DU-145 cells [27,29]. The gene discussed is BRCA1; the disease is colorectal cancer.