CX3CR1 and cancer: FKN‐induced OCP survival is likely mediated via AKT and ERK activation, as has been shown for human monocytes.(38) Recently, in analysis performed in living mice, physiological oxygen tension in CX3CR1‐expressing monocytes was determined to be 5.3%.(39) Since hypoxia increases CX3CR1 expression in some cancer cells,(40) OCP survival and differentiation under hypoxic conditions may be regulated by FKN‐CX3CR1 signaling,(41) although the mechanisms underlying these outcomes remain unknown.