The pathophysiology of endometriosis, a benign condition with certain characteristics similar to malignant tumors, may also be influenced by OPN isoforms, with overexpression in both endometriosis and adenomyosis [4,5], compared to the normal endometrium and through the activation of the phosphoinositide 3-kinases (PI3K) and nuclear factor kappa-light-chain-enhancer of activated B-cell (NF-ĸB) pathways. This evidence concerns the gene SPP1 and endometriosis.