Interestingly, these USP10 inhibitors were efficacious in selectively suppressing the growth of mutant-FLT3-expressing cells versus cells expressing wild-type FLT3, including cells resistant to FLT3 kinase inhibitors, and their growth-inhibitory effect was validated in AML preclinical models, on primary patient tumor samples and patient-derived xenografts ex vivo [265]. Here, FLT3 is linked to acute myeloid leukemia.