The singular challenge to effective cancer treatments based on previous and current strategies is the emergence of drug resistance. Accumulated evidence from decades of cancer treatments with various therapies has clearly and unequivocally highlighted that development of resistance over a “latent” time period is an inherent and default property of cancer cells [1]. As would be expected, drug resistance plays a prominent role in cancer-related mortality. How cancer-targeting effects provided by therapies become manipulated into a vehicle that initiates or promotes resistance is complex, and largely unknown. The cytotoxic nature of chemotherapy or radiotherapy, as well as specific gene or signaling abrogation offered by targeted therapies results in a tumor microenvironment that would be detrimental to “normal” non-cancer cells. Healthy cells would rapidly succumb to the damages mediated by anti-cancer therapies, however while such effects may impede tumor cells for a while, it eventually instigates cellular changes that result in resistance. The complex mechanism(s) of drug resistance is exacerbated further by the unpredictable manner of its emergence. Individualistic and highly dynamic nature of cancer cells, plus lack of standardized detection platforms complicates even further the how, the when and the where of drug resistant development [2], and poses a challenge of providing robust strategies against it.