The two alternative transcripts differently regulate BPH fecundity by binding distinct ligands and through participating in different signaling pathways; with NlGr10a promoting fecundity through AMPK and AKT-NlVg/NlVgR in fat bodies and ovaries, while NlGr10b doing so through AMPK- and AKT-NlVg signaling pathway only in fat bodies [160]. The gene discussed is AKT1; the disease is benign prostatic hyperplasia.