Transient overexpression of c‐Myc and inhibition of c‐Myc using 10058‐F4, a c‐Myc‐selective inhibitor, demonstrated a marked contribution of c‐Myc to the antitumour activity of CUDC‐907 against prostate cancer cells and suggest that c‐Myc is a potential mediator of the down‐regulation of Mcl‐1, CHK1, Wee1, RRM1 and RRM2 induced by CUDC‐907 (Figure 6H). This evidence concerns the gene CHEK1 and prostate cancer.