This is of potential importance given that disruption to the skeletal-muscle clock is sufficient to induce phenotypes common to cancer cachexia,4,26-28 including muscle atrophy and weakness, reduced regenerative capacity, fibrosis, and increased insulin resistance.17-21 Specifically, we found that FoxP1 directly binds and represses clock activator genes (e.g., Bmal1) and activates clock repressor genes (e.g., Per1, Cry1, and Cry2) and was necessary for the disruptions to circadian patterns of gene expression in skeletal muscle in response to pancreatic cancer. The gene discussed is INS; the disease is cancer.