Linebreeding in this Labrador Retriever family makes it likely that the sire and dam inherited the mutation from a common ancestor and that the affected Ginsenoside-F5 puppies are homozygous for a chromosome segment transmitted IBD. Analysis of polymorphic microsatellites showed that the regions flanking COLQ are IBD, whereas those flanking the other 2 identified candidate genes are not. Sequencing of COLQ in the Labrador Retrievers revealed a missense mutation that predicts the replacement of a conserved hydrophobic isoleucine with a hydrophilic threonine in the Cterminal domain. ColQ has 3 domains: an N-terminal proline-rich attachment domain, a collagenic central domain, and a C-terminal domain. The PRAD serves to attach the ColQ strand to an AChE tetramer. The collagen domain assembles the triple helix, while the C-terminal domain is involved in both the formation of the triple helix and anchoring of the structure to the basal lamina. In humans, mutations responsible for EAD have been identified in each domain of COLQ and have different functional consequences depending on their location. In the C-terminus, missense mutations in residues ranging from positions 342 to 452 are thought to inhibit the attachment of ColQ to the basal lamina of the muscle cell. Some C-terminus mutations may prevent the formation of the ColQ triple helix. In the affected Labrador Retrievers, localization of the esterase reaction showed a poor correlation between AChE and AChR. This finding suggests improper anchoring of ColQ to the basal lamina, or mislocalization. Insufficient muscle samples prevented us from conducting a sedimentation profile of AChE to determine the exact consequence of the I337T mutation identified. Linebreeding practices expedite the appearance of recessive diseases in purebred dog populations. The availability of genetic tests for the detection of carrier dogs allows for selective breeding to prevent widespread dissemination of the deleterious allele to the breed while maintaining genetic diversity. Because only 2 affected littermates were available for study herein, GWAS techniques could not be applied. The analysis of chromosomal inheritance patterns indicated a single functional and positional candidate gene and led to the discovery of the COLQ c.1010T.C mutation; however, our approach does not exclude the possibility that another mutation exists in a novel CMS gene. In the last few years, there have been many considerable changes in the treatment of metastatic melanoma, with the development of BRAF and MEK tyrosine kinase inhibitors and monoclonal antibody immunotherapies, such as anti CTLA-4 and anti PD-1, which have proved efficacy both in term of clinical response and overall survival. The second phenomenon involves the capacity of some anticancer agents to selectively kill or affect the biology of some immune cells. Anticancer drugs can eliminate immunosuppressive cells and enhance antitumor immune responses or mitigate Acetylcorynoline cytotoxic antitumor immunity by inducing some immunosuppressive mechanisms. In a recent work, using a mouse melanoma model B16F10, we identified DTIC immunological effect. While DTIC did not directly affect immune cells in this mouse model, we observed that DTIC triggered the expression of NKG2D ligands on tumor cells that led to activation of natural killer cells, interferon c secretion, then activation of cytotoxic T cells. We also observed that in vitro DTIC treatment enhanced NKG2D ligand expression on human melanoma cell lines.