It has been also reported that the viability of leukemia cells was reduced after the depletion of the NK-1R and that treatment with NK-1R antagonists induced an increase of apoptotic markers (annexin-V/propidium iodide), pro-apoptotic proteins (Bim, Bam, PARP, cleaved caspase-3 and 9) and the percentage of cells with sub-G1 content in these cells, whereas a decrease in anti-apoptotic proteins (Bcl-xL, Bcl-2) was also observed (Table 2) [1]. Here, BCL2L11 is linked to leukemia.