A focus on SHANK models is likely due to (1) the high prevalence of SHANK2 and SHANK3 mutations in people affected by ASD [63]; (2) SHANK2 and SHANK3, which are excitatory glutamatergic postsynaptic proteins, contain a SAM domain that directly binds zinc [41, 43, 64]; (3) synaptic localisation and expression of SHANK2 and SHANK3 are highly dependent on zinc [42–44, 64–66]; and (4) zinc deficiency dysregulates the postsynaptic SHANK scaffold, which is thought to contribute to the synaptic mechanisms underlying behavioural deficits in ASD [41, 44, 58]. Here, SHANK3 is linked to Zinc deficiency.