CTs, also known as cancer germline antigens, refer to a growing list of antigens that were initially discovered in the 1980 s–1990 s, which are specifically expressed in various tumor types6869. At present, more than 70 CTs are present families encompassing more than 140 individual members with largely unknown functions6970. Because each cancer type is associated with multiple highly expressed CTs, an effective vaccine may require the presence of multiple CTs. CTs are absent in normal humans and rodent somatic cells and are expressed only in male TGC347172737475. In this study, the mRNA expressions of seven TGC-specific AIs (including Tubb2c, Atp6v1a, Hsc70t, Fbp1, Lrrc34, Gapdhs and Dazap1) were significantly higher in testis, particularly in male germ cells, compared with that in other organs in 8-week-old mice than in 2-week-old mice. Generally, CTs can be grouped into two classes based on their chromosomal location: CTs-X are located on the X chromosome and non-X CTs are located on the autosomes. Most CTs-X are unique to primates and constitute several subfamilies of homologous genes, organized in discrete clusters along the X chromosome76. As a result of their restricted expression in an immune-privileged organ, both CTs groups represent attractive immunotherapy targets34. Antigenic CTs-derived peptides that are presented to the immune system with different human leukocyte antigen allospecificities elicit both humoral and cellular immune responses. Spontaneous humoral and cell-mediated immune responses have been demonstrated for several CTs and patients with good antibody titers often present with a better prognosis71. TGC-induced EAO involves both cellular and humoral immune responses to the autoantigen-containing AIs. Therefore, we expect that cellular and humoral immunoreactions to AIs can be identified in TGC-induced EAO. Although emerging evidence has clarified the functions of a few CTs-X in cancer, the majority remains poorly understood. In contrast, non-X CTs are fairly well conserved throughout evolution, with established roles in processes such as transformation76, chromatin remodeling34, transcriptional regulation, and cell signaling72. Thus, non-X CTs are particularly promising targets for the development of small-molecule therapeutics77. In fact, we examined whether the candidate TGC-specific AIs are upregulated in cancer cells or tumors from previous reports (Table 3). These studies suggested that Tubb2c, Pdhb, Hsc70t, Fbp1 and Gapdhs are upregulated in some cancer cells or tumors (Table 3). A list of CTs has been first manually compiled from the literature (http://www.cta.lncc.br) and the resultant CT Database contains 204 genes78. All TGC-specific AIs identified in this study are encoded on an autosomal chromosome.