Finally, we have recently shown that activating macrophages through TLR 3,4,7 leads to a pathway resulting in augmented secretion of truncated phosphorylated calreticulin, which then serves as an “eat me” signal for macrophages guiding these macrophages toward the tumor [59]; switching macrophages to the M1 phenotype should augment this, and therefore anti-CD47 in vivo anti-cancer therapies. The gene discussed is CALR; the disease is cancer.