The identification protocol is a type of zero-knowledge proof. One party (the prover) needs to prove his identity to another party (the verifier) without revealing the secret key to the verifier. One can apply the Fiat–Shamir transformation to convert an identification scheme into a signature scheme which can be used for achieving security purposes and cryptographic purposes, especially for authentication. In this paper, we recall an identification protocol, namely the RankID scheme, and show that the scheme is incorrect and insecure. Then, we proposed a more natural approach to construct the rank version of the AGS identification protocol and show that our construction overcomes the security flaws in the RankID scheme. Our proposal achieves better results when comparing the public key size, secret key size, and signature size with the existing identification schemes, such as Rank RVDC and Rank CVE schemes. Our proposal also achieves 90%, 50%, and 96% reduction for the signature size, secret key size, and public key size when compared to the Rank CVE signature scheme.

The Breakpoint Cluster Region is a protein encoded by the BCR gene with its partially discovered function to generate instructions for producing a protein and also to encode serine/threonine kinase protein. There are three Breakpoint cluster regions; major (M-bcr) which is high in CML patients, minor (m-bcr) with a 1-2% contribution in the CML, and micro (μ-bcr) which is very rare in the case of CML. The ABL1 encodes for the ABL1 protein which can function as a tyrosine kinase. The translocation of the ABL gene on chromosome 9 at the band 34 to the BCR gene on chromosome 22 at band 11 leads to the fusion of the BCR-ABL gene which is responsible for Chronic Myeloid Leukemia (CML), Acute Myeloid Leukemia (AML), and Acute Lymphoblastic Leukemia (ALL). Chromosome 22 with this hybrid gene called a Philadelphia chromosome codes for a BCR-ABL protein that enhances the activity of tyrosine kinase thereby activating numerous signaling pathways. If there is a translocation of BCR to chromosome 9, which will cause the emergence of the ABL-BCR gene (9q+). [1][4][5][6] The role of the BCR-ABL gene in CML is to increase the growth and proliferation of myeloid cells, avoid apoptosis, increase c-independent growth, induce aberrations in the cytoskeletons, etc.