In summary, our data indicate that: (a) asperolide A inhibit cell-cycle progression at the G2/M phase by decreasing the levels of CDC2, cdc25c and cyclinB; (b) asperolide A-induced G2/M arrest is mediated by p53-dependent p21 induction which is regulated by Ras/Raf/MEK/ERK signaling pathway; and (c) in vivo studies with asperolide A showed a marked inhibition of tumor growth and little toxcity. Here, RAF1 is linked to neoplasm.