Resistance mechanisms exploited by cancer cells include reluctance to perforin pore formation in target cells (reduced cell stiffness to prevent efficient perforin pore formation), changes in the cell membrane lipid order in tumor cells (42), changes in the glycosylation patterns of protein components in the cancer cell membrane (glycocode) (Figure 1), as well as secretion of cathepsin B to degrade perforins. The gene discussed is PRF1; the disease is neoplasm.