Lastly, in mouse models, the inhibition of proprotein convertase subtilisin/kexin type 9 (PCSK9), a key protein in the regulation of cholesterol metabolism, may augment immune checkpoint therapy via mechanisms involving the promotion of intratumoral T‐cell infiltration, suggesting additional potential roles for cholesterol in the tumor microenvironment which may modify (constrain) cancer growth.22 This evidence concerns the gene PCSK9 and cancer.