The human  TSC2  gene, mutations in which predispose individuals to the disease tuberous sclerosis complex (TSC), encodes a GTPase-activating protein for the GTPase RHEB. Loss of TSC2 results in constitutive activation of RHEB and its target mammalian target of rapamycin (mTOR). We have previously reported that fission yeast ( Schizosaccharomyces pombe )  Tf2  retrotransposons (hereafter  Tf2 s) are abnormally induced upon nitrogen starvation in cells lacking the  tsc2 +   gene ( Δtsc2 ), a homolog of the human  TSC2  gene, and in cells with a dominant-active mutation in the fission yeast RHEB GTPase ( rhb1-DA4 ). We report here that induction of  Tf2 s in these mutants is suppressed upon overexpression of the  cgs2 +   gene, which encodes a cAMP-specific phosphodiesterase, or upon deletion of components in the glucose/cAMP signaling pathway, namely Cyr1, Pka1, Tor1 and the stress-activated transcription factor Atf1. The results suggest that the glucose/cAMP signaling pathway is downregulated when cells are starved for nitrogen. We also show that Tf2 proteins are degraded via autophagy, which is under control of Tor2, a homolog of human mTOR. It appears that failure in the two processes, downregulation of the glucose/cAMP signaling pathway and induction of autophagy, allows abnormal induction of  Tf2 s upon nitrogen starvation in  Δtsc2  and  rhb1-DA4  cells.