I’ll have to read up on that soon. Though, the work on DUF1220 is very compelling too. Copy number increases in DUF1220 seem to be very important driver in brain evolution.
For the above reasons and because DUF1220 sequences at 1q21.1 have undergone a dramatic and evolutionarily rapid increase in copy number in humans, a model [9][14] has been developed that proposes that:
increasing DUF1220 domain dosage is a driving force behind the evolutionary expansion of the primate (and human) brain,
the instability of the 1q21.1 region has facilitated the rapid increase in DUF1220 copy number in humans, and
the evolutionary advantage of rapidly increasing DUF1220 copy number in the human genome has resulted in favoring retention of the high genomic instability of the 1q21.1 region, which, in turn, has precipitated a spectrum of recurrent human brain and developmental disorders. These include autism and schizophrenia (as discussed below) and other disorders resulting from 1q21.1 duplication syndrome and 1q21.1 deletion syndrome.[9]
From this perspective, disease-associated 1q21.1 CNVs may be the price the human species paid, and continues to pay, for the adaptive benefit of having large numbers of DUF1220 copies in its genome.[9][14]
Olduvai domain - Wikipedia
This is all pretty interesting and compelling work.
It is worth explaining that brain size is not correlated with intelligence, rather it is the number of neurons that is important. The only order where brain size is correlated with number of neurons is primates. In all other orders (as far as I know), brains size varies, but the number of neurons does not increase with bigger brains.
Lest this be misinterpreted, I’m talking about variance between species, not within species. Humans with different size brains can all be equally intelligent (within species variance).
Any how, I’ll circle back once I get a chance to read the new paper.