In CUR-treated cells the ERK (extracellular signal-regulated kinases)1/ERK2 mitogen-activated protein (MAP) kinases activity was down-regulated [43] and in combination with mitomycin C (MMC) there was enhanced G1 arrest with resultant inhibition of cancer cell proliferation and cycle progression in vitro and in vivo via the p38-MAPK pathway [44]. The gene discussed is MAPK1; the disease is cancer.