PCSK9 and neoplasm: Li et al. found that PCSK9 interacts with MHC I and promotes its trafficking to the lysosomes and subsequent degradation, while blocking its recycling back to the membrane.1 As a consequence, cells expressing PCSK9 have reduced levels of surface MHC I and thus escape CTL recognition, while PCSK9 deficiency or inhibition promote tumor-T cell interaction (Fig. 1).