The major canonical pathway upregulated in a dose-dependent manner in both cell lines was apoptosis signalling (Fig. S6, ESI†), consistent with sulforaphane's ability to induce apoptosis in numerous cancer cell lines at elevated concentrations.19 In both cell lines a common apoptosis signalling target was NF-κB subunits (Fig. S7, ESI†). The gene discussed is NFKB1; the disease is cancer.