SOAT1 and Thrombocytopenia: The IFN-I treatment could enhance the cytotoxic function of the patient’s NK and CD8+ T cells,30,31 inhibited hematopoietic function and caused the alteration of peripheral blood neutrophils and thrombocytopenia.32 In addition, IFN-I treatment directly or indirectly triggered the signal cascade of JAK-STAT, MAPK, PI3K, and NF-κB pathways to participate in the regulation of interferon response.33–35 Therefore, the changes at the transcriptome levels of our patients might partially come from interferon therapy.