One of the major findings concerning MJ is that it was able to detach HK1 and HK2 from VDAC in a time- and dose-dependent manner in the mitochondrial fraction of murine colon carcinoma CT-36 cells, human leukemic Molt-4 and murine BCL1 cells, and murine B16 melanoma tumor cells by specifically binding to HK2, as judged by HK immunochemical, surface plasmon resonance and planar lipid bilayer VDAC-activity analyses, without inhibiting the kinase activity [30]. The gene discussed is HK2; the disease is neoplasm.