By suppressing the formation and accumulation of potential inducers of β-cell damage in diabetic rats (detected as a decrease in CML-containing species in the pancreas), Ld administration activated prosurvival CXCL12/Akt signaling and the proliferative pathway, observed as the increased presence of PCNA-containing β-cells. The gene discussed is AKT1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.