For example, ID1 and ID2 appear to inhibit MYOD and MYF5 action but not that of MYOG or MRF4, while ID3 showed a weak inhibition of all MRFs32 suggesting that ID3 can function both in early and late myogenic differentiation if it is expressed, as occurs in cells overexpressing C/EBPβ and in our model of cancer cachexia. This evidence concerns the gene MYOD1 and cancer.