Scientists have developed various methods for the identifying of novel anti-CRISPR (Acr). Among them, the guilt-by-association is the most classic one which used the conserved anti-CRISPR associated proteins (Aca) as a bait. But this method is limited by the lacking characterized of Acrs and Acas in the archaea viruses. We analyzed all the known Acrs of archaea viruses, found that all the genes expressed immediately after infection and their promoter regions were identical. Based on this founding, we guess all the anti-defense genes may have this identical promoter. The analysis of 57 archaea virus and 4 metagenome-assembled genomes discovered 365 anti-defense related genes. Based on the genetic tools which developed by our lab, we cloned the 6 candidates of Sulfolobus islandicus filamentous virus 2 (SIFV2) to the Sulfolobus islandicus LAL14/1 ΔCas6 I-D and used several SIRV2 mutations (SIRV2MΔacrIA, SIRV2MΔacrIIIB1/ΔacrIA) to infect the cells. Only SIRV2MΔacrIA infected the gp15 expressed strains caused the growth retardation. Further spot assay and plaque assay showed the viruses replication after the infection. So we found the first Acr for the subtype I-A CRISPR-Cas system. In SMV1, there is a genes gp44 which also is the homologue of the type II antitoxin gene belonging to the PhD-Doc family toxin-antitoxin genes. We constructed plasmids which encode the LAL14/1 PhD-Doc pair SiL_0730 (PhD) /SiL_0730 (Doc) or gp44 /SiL_0730 (Doc) which were transformed to the LAL14/1, showed that the gp44y can inhibit the SiL_0730 from the archaea. Later the experimental evidence showed that gp44 has the same function of type II antitoxin which can inhibit the archaeal abortive infection system. We also identified the novel Acas by this approach which can be used for further Acrs discovery. The Acrs are not identical which also limited the identity of the novel Acr. AcrID1 encoded by the SIRV2 was identified as an inhibitor for the subtype I-D CRISPR-Cas system. But the protein sequence searches found approximately 50 homologues of AcrID1 in the viruses infected the hyperthermophilic crenarchaeota strains. 12 of them belong to SIRV2. So we asked that why the SIRV encode so many AcrID1 homologues. We predicted their structure by the Alphafold2, the structure and also the electrostatics of most homologues were not similar to the AcrID1. We tried to purify the proteins from the E.coli, only 6 were obtained. Late we tested their inhibitory for the I-D effector, only the gp51 blocked the target dsDNA cleavage. Subsequently, further ssDNA binding assay gave us the evidence that gp51 blocked the ssDNA binding activity of backbone. Most of homologues are functional unknown genes, but we guess they may be Acrs for other subtypes of I-D CRISPR-Cas systems. But the function explore of them need more I-D systems were discovered.