The pathway analysis indicated alterations in PI3K/Akt [75], [76], MYC [68], [70], [71] and NF-κB [72] signaling pathways, and potential critical roles for TGFA[77], [78], ErbB2[7], [79], [80], [81], and IL-1/IL-1R[82], [83], [84] which may promote angiogenesis, tumor growth, and metastasis and hence cause the aggressive phenotype observed in young women. The gene discussed is AKT1; the disease is neoplasm.