Moreover, the deletion of ABCG1 in macrophages derived from bladder carcinoma and melanoma caused free cholesterol intracellular accumulation and an increase in NF-kB p65 phosphorylation that promotes TAM re-polarization to an M1 phenotype, thus suggesting how, in this context, ABCG1 deficiency is associated with p65 activation to counteract tumor growth [176]. This evidence concerns the gene ABCG1 and urinary bladder carcinoma.