Finally, consistent with the gain and loss of function tests (Figure 2), increased activities of the TFAM promoter (Figure 4C) demonstrated NFκB2′s regulatory role in the gene expression of TFAM, supporting our hypothesis that TKI-increased NFκB2 can regulate both mitochondrial and nuclear transcription systems directly (through promoting LSP- and HSP1-mediated transcription) and indirectly (through increasing TFAM) to undergo mitochondrial biogenesis and metabolic reprogramming to support AML relapse (Figure 4D). The gene discussed is SYPL1; the disease is acute myeloid leukemia.