Together with normal tolerance to exogenous insulin (Figure 1B) and glucose (not shown), normal fasting insulinemia and random glycemia (Table 1) demonstrated persistent insulin sensitivity in Ldlr−/−VECadCre+Cc1fl/fl mice, as expected of the Ldlr−/− background, which does not significantly cause/accelerate insulin resistance in the absence of other genetic factors [5]. This evidence concerns the gene INS and Insulin resistance.