Socs44A increases activity of EGFR signaling. The ectopic wing vein phenotype of Socs44A misexpression (A) is rescued by reduction of Egfr (B), Sos (C) or Ras85D (D), positive effectors of EGFR signaling. In contrast, reduction of argos, a negative regulator of EGFR signaling, enhances the Socs44A misexpression phenotype (E). The argos allele combined with en-GAL have no effect on venation without the UAS-Socs44A transgene (F). Certain heteroallelic Egfr mutants possess a distinct wing vein phenotype, whereby the anterior crossvein and the central portion of L4 is missing (G, arrows). Engrailed-driven misexpression of argos has a similar phenotype (H and J). Concurrent misexpression of Socs44A antagonizes argos misexpression to restore near normal wing venation (I and K). The designation "2xUAS-argos" refers to presence of 2 total copies of the transgene in the genome.