These results indicated that the significant association of the HLA-A locus with susceptibility to CM-SJS/TEN with SOC was caused by the regulatory effects of primary functional polymorphisms (including SNVs, INDELs, and SVs) located near HLA-A; further, the expression level of HLA-A was up-regulated by the disease susceptibility-associated HLA-A polymorphism. This evidence concerns the gene HLA-A and cutaneous mastocytosis.