Noncanonical NRF2 activation by the PI3K/AKT signaling was also observed in HCT-116 colorectal cancer cells treated with benzyl isothiocyanate (BITC), an aromatic compound known to induce the accumulation of NRF2 and other autophagic molecules, since when PI3K/AKT inhibitors were coadministered, the sensitivity of HCT-116 cells to BITC was greatly enhanced [244]. The gene discussed is AKT1; the disease is colorectal cancer.