Given that the RASopathy-associated mutation T102R is in close proximity to S105 and showed an even stronger phenotype in a cell competition assay than the phosphomimetic mutant SPRED1-S105D, it is plausible to assume that T102 in the EVH-1 (Ena/VASP Homology 1) domain of SPRED1 is also contributing to the above regulation [11,81]. This evidence concerns the gene SPRED1 and RASopathy.