Therefore, it can be hypothesized that genes involved in the process of cell proliferation and survival may evolve, in resistant conditions, to be highly correlated with the genes in the glucose deprivation response network in order to establish an alternate mechanism of glucose uptake in cancer cells, even though the inhibiting effects of lapatinib abrogated their dependencies on EGFR/ErbB2 signaling in sensitive conditions (See Fig 1 of [20]). The gene discussed is EGFR; the disease is cancer.