Our previous studies have revealed significant upregulation of four complement system activators (FB and C3 in AP; C1r and C1s in the classical pathway) plus two complement inhibitors, complement factor I (FI) and complement factor H (FH), in cSCC cell lines in vitro as well as in tumor cells in cSCC in vivo, when compared with normal human epidermal keratinocytes (NHEKs) and normal skin, respectively [25,26,27,28,29,30]. The gene discussed is C3; the disease is neoplasm.