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Exposure to BPA induces metabolic disorders in the paternal mice, which are then transmitted to offspring, leading to late\u2010onset MetS. Mechanistically, BPA upregulates Srebf1, which in turn promotes the Pparg\u2010dependent transcription of <jats:italic>Dicer1<\/jats:italic> in spermatocytes, increasing the levels of multiple sperm microRNAs (miRNAs). Several of these miRNAs are highly expressed in a synchronized manner in liver of the offspring. miR149\u20105p, miR150\u20105p, and miR700\u20105p target a specific region in the Lepr 3\u2032UTR, termed \u201cSMITE\u201d (\u201c<jats:styled-content>S<\/jats:styled-content>everal <jats:styled-content>Mi<\/jats:styled-content>RNAs <jats:styled-content>T<\/jats:styled-content>argeting <jats:styled-content>E<\/jats:styled-content>lements\u201d), to negatively regulate Lepr. These <jats:styled-content>i<\/jats:styled-content>nherited <jats:styled-content>a<\/jats:styled-content>nti\u2010<jats:styled-content>L<\/jats:styled-content>epr miRNAs, also referred to <jats:styled-content>i<\/jats:styled-content>nherited <jats:styled-content>a<\/jats:styled-content>nti\u2010<jats:styled-content>L<\/jats:styled-content>epr miRNAs (IAL\u2010miRs), modulate hepatic steatosis, and insulin signaling through the Lepr regulatory Igfbp2, Egfr, and Ampk. Furthermore, IAL\u2010miRs inhibit Ccnd1 not only via binding to \u201cSMITE\u201d but also via Lepr\u2013Igfbp2 axis, which contribute to hepatocyte senescence. These pathological processes interact in a self\u2010reinforcing cycle, worsening MetS in the paternal BPA\u2010exposed offspring. 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