Experimental manipulation of G1 length through Cdk4/CyclinD1 overexpression or shRNA depletion alters the balance of progenitor self-renewal and neurogenesis, altering surface area of the postnatal cerebral cortex (Lange et al. 2009); thus, a role for CDK4 in regulating G1 progression in neurogenesis would be sufficient to explain microcephaly. The gene discussed is CCND1; the disease is microcephaly.