Since SR-B1 does not appear to be involved in mediating this protective effect (Figure 1A), we hypothesized that myeloid cells deficient in either ABCA1, ABCG1 or both, which in multiple studies have previously been noted to have an inflammatory gene signature [2, 16, 26–28], might be protective in a B16F10 melanoma tumor model. Here, ABCA1 is linked to neoplasm.