To investigate the roles of the ISR in this cancer, we took advantage of our ability to culture the tumor-initiating stem cells from mouse skin SCCs and generated primary, clonal cell lines in which the endogenous eIF2α alleles were replaced by myc-epitope tagged but otherwise fully functional versions of either wild-type eIF2α or eIF2α-S51A (ISR-null). The gene discussed is EIF2A; the disease is neoplasm.