Based on these results, we conclude that (a) uncharacterized constituent(s) of GL may interact additively or synergistically to inhibit the viability of human breast cancer cells, (b) a normal human mammary epithelial cell line is significantly more resistant to the growth inhibition by GL, and (c) the growth inhibition of human breast cancer cells by GL is not influenced by the estrogen receptor expression. The gene discussed is ESR1; the disease is breast cancer.