To assess this possibility, we first analyzed the combinatorial effect of the potent non-covalent inhibitor calmidazolium (CMZ) and the PP2A activating SMAP, DT-061 (Scheme 1), on the growth of KRAS mutant MDA-MB-231 breast and NCI-H358 lung cancer cell 3D spheroids, as well as BRAF mutant A375 skin cancer cell spheroids. The gene discussed is BRAF; the disease is lung carcinoma.