The analysis of deep-infiltrating endometriotic lesions associated with cancer showed the frequent occurrence of somatic mutations (observed in 79% of cases); 26% of cases displayed driver mutations at the level of ARID1A, PIK3CA, KRAS or PPP2R1A genes (Figure 2); importantly, all the tested somatic mutations appeared to be confined at the level of the epithelial compartment of endometriotic lesions [136]. This evidence concerns the gene KRAS and cancer.