INS and diabetes mellitus: It is possible that (i) apoA-II expression in the transgenic mice triggers developmental effects on insulin secretion, or (ii) apoA-II induces beta-cell proliferation after adenoviral transduction, as demonstrated in diabetes-resistant B6-ob/ob mice, where adenoviral overexpression of apoA-II contributed to the adaptive islet hyperplasia and, thus, prevented these mice from severe diabetes [72].