Further phenotypic screens in several other cancer cells too may confirm CaMK2A enhanced activation by Bacoside A to be useful for treatment of cancers as well as for targeting the quiescent tumor initiating populations, as it functions on the common mechanism of generation of high hydrostatic stress via CaMK2A-pCaMK2A-high intracellular calcium-excessive cell drinking pathway (please see the mechanistic model in Figure 11C). The gene discussed is CAMK2A; the disease is neoplasm.