The emerging paradigm from the studies by Zamanian-Daryoush and that of Sag et al., is that TAMs can be converted from an M2-like to an M1-like phenotype by either a hard-wiring to an M1 anti-tumor phenotype through loss of cholesterol/phospholipid transporter ABCG1 (Sag et al., 2015) and perhaps ABCA1 and SR-B1 or in response to increased apoA1/HDL levels; which by unknown mechanisms alters immune responses to factors within the tumor microenvironment and promotes the accumulation of TAMs with an M1-like phenotype at the expense of TAMs with an immune suppressive M2-like phenotype. This evidence concerns the gene ABCG1 and neoplasm.