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Here, we show that EGF and HRG induce different modes of G1\/S progression in ErbB2\u2010amplified BT474 breast cancer cells. Unexpectedly, HRG, despite activating the more potent ErbB2\u2010ErbB3 heterodimer, failed to accelerate G1\/S progression; instead, EGF promoted earlier passage through the restriction point and faster S\u2010phase entry. Mechanistically, EGF drove rapid and coordinated cell\u2010cycle progression through ERK\u2010FOS signaling, whereas HRG induced sustained MYC activity, elevated transcriptional heterogeneity, and caused extensive rewiring of cell\u2010cycle regulatory networks. 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