There are two possibilities why we could not observe staining of CaV1.2 by AML: either interaction with the channel does not lead to fluorescence increase, presumably because AML takes the molecular conformation with lower fluorescence emission than in a stabilized form in BSA/HSA solutions, or the density of receptors is too low for the detection and is masked by receptor-independent staining. This evidence concerns the gene CACNA1C and acute myeloid leukemia.