Furthermore, analysis of the tumor response of C57BL/6.Psl1Bdba and C57BL/6.Psl1Edba subcongenic strains (Figure 1) initiated with 2.5 μmol of MNNG and promoted twice weekly with 13.6 nmol of TPA suggested that Psl1 consisted of at least two subloci, Psl1.1 and Psl1.2, that modify susceptibility to skin tumor promotion (Abel et al. 2010). The gene discussed is SPPL2B; the disease is neoplasm.