This view is supported by the following features shared by both OSCCHT and malignant rhabdoid tumor: occasional familial occurrence, frequent hypercalcemia, and immunohistochemical polyphenotypia.[12] Additionally, in vivo studies have revealed that the simultaneous presence of c-Met in 41% of OSCCHT-1 cells, reduced proliferative capacity, and decreased tumor size are observed after siRNA-mediated c-Met knockdown in OSCCHT-1 cells, demonstrating that in vivo inhibition of these pathways contributes to attenuation of OSCCHT tumor growth.[17]. The gene discussed is MET; the disease is rhabdoid tumor.