In this study, many new mutations, generally insertions, were detected in different exons. These mutations contribute to significant changes in the protein structure of hBDs. hBD-1 mutations and mutation1 of hBD-3 are the most damaging because they lead to truncated pre-proteins with no predicted mature hBD-1 protein synthesis. hBD-3 mutation 2 protein is greatly destabilized because of the absence of a disulfide bridge caused by the substitution of Cys63.If none of the new points satisfies the distance requirement, the one that is farthest away from other points is selected. It is well-established that aPL antibodies amplify platelet activation, which was verified in this investigation. Activated platelets expose several molecules including phosphatidylserine and chondroitinsulfate which support binding of C1q and subsequent complement activation. DNA recombination technologies such as the Cre/LoxP system have advanced and refined the analysis of gene and cell functions in mice. In contrast to classical in vivo strategies, which result in a complete deletion of gene function in the whole organism, this conditional gene targeting technology enables a cell type-specific deletion of genes by driving the expression of Cre recombinase under the control of a cell type-specific promoter. In addition, the Cre/LoxP system has been used for fate mapping and for cell ablation in vivo. Firstly, aPL antibodies contribute to platelet activation-mediated complement deposition. Supporting the hypothesis of platelet activation being sufficient to allow complement activation we observed that sera from healthy individuals supported complement activation on the surface of activated platelets also confirming observations in one of our previous studies.