A recent study from Dr. T. Lawrence's lab has demonstrated, in a peritoneal ovarian cancer model, that LPMs were progressively replaced by monocyte‐derived macrophages, that gradually upregulated genes related to cholesterol metabolism and reverse cholesterol efflux.[87] Indeed, tumor cells promoted cholesterol efflux in monocyte‐derived macrophages that drove IL‐4‐mediated, STAT6/PI3K‐dependent, macrophage reprogramming, involving increased arginine metabolism, and inhibition of IFNγ‐induced gene expression, that promoted tumor progression. This evidence concerns the gene STAT6 and neoplasm.