CamK-A is able to do so by activating the Ca2+/calmodulin-dependent kinase PNCK, leading to the phosphorylation of IκBα, which activates NF-κB, which remodels the tumor microenvironment in several ways by promoting macrophage recruitment, angiogenesis, and tumor growth. This evidence concerns the gene NFKB1 and neoplasm.