Mouse PSC have also been shown to be susceptible to alternative complement pathway-mediated killing that affects their ability to form teratomas, in an inverse correlation to the number of PSC transplanted as complement could block teratoma formation by 1 × 105 but not with 1 × 106 PSC, and the C3−/− mice could form teratomas much faster than the C3+/+ mice in part due to deficiency of sialic acid in the PSC (45). This evidence concerns the gene C3 and teratoma.