Our study pointed to the interesting mechanism of cholesterol metabolism in the interactions of CD16+ neutrophils with NK cells, adding to the other known NK cell‐related inhibitory mechanisms in cancer.[65, 66] In CRC, we found that cholesterol is accumulated in CD16+ neutrophils through the upregulation of CD36 and LRP1, which we believe could influence the tumor microenvironment in one of two ways. The gene discussed is CD36; the disease is colorectal carcinoma.