maintains that the science of the studies is sound, and freely admits that a direct link between these particular genes and either cognition or intelligence has not been clearly established. Lahn is now engaging himself with other areas of study. Later studies have not found those gene variants to be associated with mental ability or cognition. Later genetic association studies by Mekel-Bobrov et al. and Evans et al. also reported that the genotype for MCPH1 was under positive selection. An analysis by Timpson et al., found "no meaningful associations with brain size and various cognitive measures". A later 2010 study by Rimol et al. demonstrated a link between brain size and structure and two microcephaly genes, MCPH1 (only in females) and CDK5RAP2 (only in males). In contrast to previous studies, which only considered small numbers of exonic single nucleotide polymorphisms (SNPs) and did not investigate sex-specific effects, this study used microarray technology to genotype a range of SNPs associated with all four MCPH genes, including upstream and downstream regulatory elements, and allowed for separate effects for males and females. Model organisms Model organisms have been used in the study of MCPH1 function. A conditional knockout mouse line, called Mcph1tm1a(EUCOMM)Wtsi was generated as part of the International Knockout Mouse Consortium program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists. Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion. Twenty four tests were carried out on mutant mice and six significant abnormalities were observed. Homozygous mutant animals were infertile, did not have a pinna reflex, had a moderate degree of hearing impairment, abnormal cornea morphology, lens morphology and cataracts, and displayed chromosomal instability in a micronucleus test. MCPH1 is involved in the ATM and ATR-mediated DNA damage response that includes repair of DNA damages. In humans, neurodevelopmental disorders including microcephaly are often associated with a deficient DNA damage response. In mice lacking MCPH1, DNA damaging ionizing radiation causes massive apoptosis in the neocortex. Loss of Mcph1 gene function in mice compromises homologous recombinational repair of DNA damages, thus increasing genomic instability. MCPH1 facilitation of the DNA damage response appears to be necessary for proper neuroprogenitor cell expansion and differentiation. Other MCPH genes In addition to MCPH1, other genes have been designated MCPH genes based on their role in brain size. These include WDR62 (MCPH2), CDK5RAP2 (MCPH3), KNL1 (MCPH4),