HES1 and Merkel cell skin cancer: found that tumor cells evaded recognition by CD8+ T cells by selectively downregulating the expression of specific HLA genes, resulting in acquired adoptive cellular immunotherapy and ICI therapy resistance, through scRNA-seq in two metastatic MCC patients (77), while the histone deacetylase inhibitor domatinostat can reverse this effect by restoring HLA gene expression on MCC cells (78), and cause decreased cell viability and apoptosis through suppressing the transcription factor HES1 (79).