While this observation prompted those authors to link reduced Ccdn1 levels to apoptosis, cell cycle delay, and tumorigenesis (Fazio et al. 2016), our findings formally raise the possibility that CdLS patient cell survival may result in part from Ccnd1 reduction, a model supported by findings that nipblb/smc1a reduction does not necessarily produce Ccnd1 down regulation (Fazio et al. 2016). The gene discussed is SMC1A; the disease is Cornelia de Lange syndrome.