Deduced mechanisms responsible for the escape of HSPCs from cytotoxic T cells specific for autoantigens presented by HLA-B4002. Normal HSPCs are killed by CTLs that recognize autoantigens presented by HLA-B4002 (A), but HSPCs that have undergone various mutations of HLA-B4002 escape this CTL attack in different ways, such as via the complete loss of HLA-B4002 expression due to 6pLOH, nonsense and frameshift mutations, or deactivation of splice sites (B), partial loss of HLA-B4002 protein due to alternative splice site formation (C), and failure of CD8⁺ T-cell binding to the α-3 domain of HLA-B4002 (D).