Recent evidence via novel small molecule intervention and genetic ablation has shown that loss of oncogenic KRAS function, for example, is prone to initial tumor volume loss followed by tumor regrowth, either as a consequence of cancer cell heterogeneity in KRAS dependency or the presence of highly KRAS-dependent cells harboring the ability to undergo a stress-induced clonal escape mechanism mediated through advantageous functional alterations [28–32]. Here, KRAS is linked to neoplasm.