Immunohistochemical (IHC) analyses with anti-DHHC9, anti-GLUT1, anti-Ki67, and anti-cleaved PARP1 antibodies revealed that tumor samples derived from U87 cells with the knockout of endogenous DHHC9 or GLUT1 displayed no expression of DHHC9 or GLUT1, respectively, had decreased expression of proliferation marker Ki67 and increased positive rate of apoptotic marker cleaved PARP1 (Fig. 5c). This evidence concerns the gene PARP1 and neoplasm.