Specifically, in two complementary colorectal cancer epithelial models, HT 29 and Caco 2, statin exposure is associated with coordinated attenuation of ERK1 and ERK2 pathway output, including reduced ERK abundance and phosphorylation, suppression of an ERK-responsive transcriptional target, and concordant reduction in tumour necrosis factor alpha at both transcript and secreted protein levels. The gene discussed is MAPK1; the disease is colorectal cancer.