Among the mechanisms involved, a modulation by n-3 LC-PUFA of the mammary tumor microenvironment [21], a reduction of M-CSF released by tumor cells [44], a decrease in CD44 (protein associated with epithelial mesenchymal transdifferentiation implicated in the metastatic potential) [22], or a modulation of the prosurvival/proliferative effects of estrogen [45] have been demonstrated. This evidence concerns the gene CSF1 and neoplasm.