We examined reasons for pupal death following expression of certain transgenes with predominantly eye-disc expressing GMR-GAL4 or sev-GAL4 drivers in Drosophila. GMR-GAL4 or sev-GAL4 driven expression of activated Ras producing UAS-Ras1V12 transgene caused early (~23-25 Hr pupation) and late pupal death, respectively. Co-expression of UAS-hsrω-RNAi transgene or EP3037 (lncRNA hsrω gene's GAL4-driven over-expressing allele) with sev-GAL4>UAS-Ras1V12 advanced death to 23-25 Hr after pupation. We show that the normal ecdysone surge was absent in 23 Hr old GMR-GAL4>UAS-Ras1V12 pupae or those co-expressing sev-GAL4>UAS-Ras1V12 with hsrω-RNAi or EP3037. Microarray and immunostaining data revealed Dilp8 and several members of JNK pathway to be elevated in >16 Hr old GMR-GAL4>UAS-Ras1V12, sev-GAL4>UAS-Ras1V12 hsrω-RNAi and sev-GAL4>UAS-Ras1V12 EP3037 pupae. Down- or up-regulation of hsrω transcripts exaggerates Ras signalling resulting in elevated JNK signalling and consequent more Dilp8 secretion by the affected eye discs. We show for the first time that the intriguing early pupal death following expression of certain transgenes by the predominantly eye-specific GMR-GAL4 or sev-GAL4 drivers activates JNK-mediated Dilp8 secretion which reduces post-pupal ecdysone and thus leads to pupal death.