Park et al. reported that CD45 overexpression enhanced stemness and therapy-resistant phenotype of colorectal cancer cells, as a result of its phosphatase activity promoting Wnt transcription by dephosphorylating and stabilizing the β-catenin protein.45 In addition, the extracellular domain of CD45 has complex interactions with other molecules such as BTN3A1 and galectin-1 that can be secreted in the circulation.46,47 These interactions may change the phosphatase activity of CD45, thus regulating the downstream signaling. Here, BTN3A1 is linked to colorectal cancer.