The findings suggest that C3 activation products, such as iC3b, C3b, and C3d, rather than anaphylatoxins C3a and C5a, can promote tumor growth and epithelial hyperplasia by interacting with the receptor CR3 on infiltrating myeloid cells, suggesting that complement C3 drives inflammatory skin carcinogenesis independently of complement C5 [58]. This evidence concerns the gene C3 and neoplasm.