anticancer property of indole-3-carbinol is driven by specific targeting of oncogenic pathways. In two different studies using xenografted mouse model of melanoma, they observed that subcutaneous injection of indole-3-carbinol could bring down tumor burden significantly. The underlying molecular mechanism of this anti-tumor effect was found to be by the specific inhibition of activity of oncogenic BRAFV600E in tumors that harbored the mutation. However, in tumors that expressed wild type BRAF, indole-3-carbinol did not cause any comparable antiproliferative effect. Additionally indole-3-carbinol did not cause antiproliferation even in normal epidermal melanocytes underscoring the specificity and selectivity of its action. Kundu et al. further showed that inhibition of BRAF V600E activity by indole-3-carbinol resulted in downregulation of MITF-M by downstream signaling which caused a G1 cell cycle arrest leading to the observed antiproliferative effect. In a second study Kundu et al. showed that in melanoma cells where PTEN is downregulated, indole-3-carbinol directly interacts with NEDD41 to prevent PTEN ubiquitination and subsequent proteasomal degradation. This results in stabilization of PTEN and inhibition of proliferation by downstream AKT signaling. Overall scientific evidence shows that in melanoma, indole-3-carbinol specifically inhibits the two most commonly associated driver mutation signaling pathways to cause proliferation, a fact that can be used to design clinical trial to treat human patients with indole-3-carbinol in future. Systemic lupus erythematosus Indole-3-carbinol can shift estrogen metabolism towards less estrogenic metabolites. Systemic lupus erythematosus (SLE, or lupus), an autoimmune disease, is associated with estrogen. In a study using mice bred to develop lupus, indole-3-carbinol was fed to one group while another group was fed a standard mouse diet; the group fed the indole-3-carbinol diet lived longer and had fewer signs of disease. Another study of lupus-prone mice with indole-3-carbinol defined the mechanism for the improvement of their disease to be due to sequential blocks in the development of B and T cells of these mice. The maturation arrests resulted in a fall in autoantibody production, thought to be a crucial component of lupus causation. In addition, I3C supplementation of the disease prone mice led to a normalization of their T cell function. Women with lupus can manifest a metabolic response to indole-3-carbinol and might also benefit from its antiestrogenic effects. Clinical trials are currently underway to determine the efficacy of treating human patients with lupus using indole-3-carbinol. Effect in recurrent respiratory papillomatosis There is evidence suggesting that indole-3-carbinol may have an effect on human papillomavirus-infected