(40) reported a review about the CD200 expression and function in the tumor microenvironment as well as alternative strategies for potential neutralization of CD200 in human cancers, indicating that a probable explanation for the observed shortcomings in the samalizumab phase I trial could be the alternative mechanisms for the CD200 pro-tumorigenic role, beyond direct suppression of anti-tumor T cell responses, such as engagement of the CD200-CD200R axis, transcriptional mechanisms related to the cleaved cytoplasmic tail and ectodomain shedding. The gene discussed is CD200; the disease is neoplasm.