Primary resistance to immune checkpoint blockade antibodies such as anti-PD1/PD-L1 or anti-CTLA4 is mainly associated with a lack of antitumor effector T cells including Th1 CD4 and CTLs, which correlates with low tumor mutational burden, inefficient presentation of tumor antigen(s), microbiota dysbiosis, and/or deficiency in IFNγ-mediated signaling in the tumors [29,30,31,32,33,34,35]. This evidence concerns the gene CTLA4 and neoplasm.