In particular, three nonexclusive processes were suggested: (i) tumor cells secreted C1r, C1s, C3, C4, and C5, which, in association with C1q macrophage production, led to the canonical complement cascade activation; (ii) C1s modified the tumor cell transcription program and phenotype and promoted their proliferation and survival; (iii) a complex synergic interaction between the C1q-producing tumor cells and T cells was observed. The gene discussed is C4A; the disease is neoplasm.