To investigate the effect of these ABPs in Src-induced proliferation, we first screened for those that affect the pro-growth function of Src in Drosophila, as this organism contains only one family member for each of these ABPs (Supplementary Table 2), reducing the risk of gene redundancy. As expected, distal wing discs overexpressing Drosophila Src oncogene at 64B (Src64B) together with the Caspase inhibitor p35 and Green fluorescent protein (GFP) using the the Nubbin-Gal4 (Nub-Gal4) driver were significantly bigger than control discs expressing GFP only (Fig. 4a,b). Strikingly, replacing UAS-GFP by a UAS construct expressing double-strand RNA (dsRNA) directed against EVL/Ena in Nub>Src/p35 wing discs fully suppressed tissue overgrowth (Fig. 4a,b and Supplementary Table 2). In contrast, knocking down ACTR3/Arp3, ARPC5L/Arpc5, DST/Shot, FHOD3/Fhos or TPM2/Tm2 enhanced the overgrowth of Nub>Src/p35-expressing wing discs (Supplementary Table 2 and Supplementary Fig. 5). In the converse experiments, overexpressing EVL/Ena strongly enhanced Src-induced tissue overgrowth (Fig. 4a,b and Supplementary Table 2), while overexpressing ACTR3/Arp3 or DST/Shot or an activated form of Fhos deleted of the conserved C terminal basic cluster (EGFP-Fhos-βB) reduced the overgrowth of these tissues (Supplementary Table 2 and Supplementary Fig. 5). These observations suggest that EVL/Ena promotes Src/p35-induced tissue overgrowth, while ACTR3/Arp3, ARPC5L/Arpc5, DST/Shot, FHOD3/Fhos and TPM2/Tm2 could have the opposite effect.