We found that transient (<15 min) ERK1/2 phosphorylation contributed to cancer proliferation,8 whereas sustained (>15 min) ERK1/2 phosphorylation resulted in growth inhibition and apoptosis.9 We found that SFN induced apoptosis by activating ERK1/2 in human glioblastoma cells, and we just reported that SFN-Cys inhibited invasion by persistent ERK1/2 phosphorylation in human prostate cancer cells. Here, MAPK3 is linked to cancer.