Transcriptome sequencing and subsequent qPCR and western blot validation indicated that CD37 deficiency in AML LSCs leads to reduced AKT phosphorylation, decreased BCL2 expression, and increased p27 expression, which was consistent with the pro-apoptotic phenotype observed in CD37−/− AML LSCs. The gene discussed is CDKN1B; the disease is acute myeloid leukemia.