We found little evidence for complosome activity in cancer, but rather for NCP-mediated activation of intracellular signaling pathways, suppressing tumors in certain settings (e.g., for C1q, by activating WWOX in breast and prostate cancer cells (22, 23), and more commonly driving malignancy by stromal interactions, receptor signaling, and matrix remodeling, (e.g. C1q by engaging receptors as DDR1 and HA to activate MAPK signaling or modulate MMPs, fostering tumor aggression) (47, 48). Here, DDR1 is linked to neoplasm.