Mutation or depletion of SMC1A in human cells generates W-CIN5, 8, and we demonstrate for the first time, that it induces premature senescence and SASP through expression of CDKN1A and CDKN2A. Senescence induction through SMC1A deficiency provides a possible explanation for the accelerated aging phenotype presented by patients affected by the cohesinopathy Cornelia de Lange Syndrome (CdLS)52. This evidence concerns the gene SMC1A and Cornelia de Lange syndrome.