Flt3 degradation mediated by HBX19818 and P22077 showed high efficiency in treatment of AML cell lines and patient-derived AML xenograft resistant to FLT3 kinase inhibitors, highlighting USP10 inhibition as a potential target for Flt3 kinase inhibitor-resistant AML patients [73]. This evidence concerns the gene USP10 and acute myeloid leukemia.