MYC and neoplasm: Both MYC and its neuronally-expressed paralogue, MYCN, can prevent transcription-replication conflicts (TRCs) and limit replication-associated DNA damage20,21,23,24, suggesting that TRCs or DNA damage arising during S-phase cause the slow progression of MYC-depleted PDAC cells through S-phase and that factors that prevent TRCs or limit the DNA damage during S-phase may be critical for tumor growth.