While mutations in four genes encoding Forkhead (Fkh/Fox) domain transcription factors (TFs) have been linked to human congenital heart defects and eight Fkh TFs are required for proper cardiac development in mammals, little is known about the molecular mechanisms or the downstream target genes by which these Fkh TF-mediated cardiogenic functions are brought about. Our prior work identified the cardiogenic roles of two Drosophila Fkh genes, jumeau (jumu) and Checkpoint suppressor homologue (CHES-1-like). Mutations in these genes result in numerous heart defects, including disruptive changes in cardiac cell types and numbers, errors in cardiac progenitor cell specification and division, and defects in cardiac cell position. Furthermore, Fkh TF binding sites are significantly enriched in combination with those of other known cardiogenic TFs in the enhancers of cardiac genes. Collectively, these results indicate that these two Fkh TFs integrate diverse cardiogenic processes by regulating a large number of downstream target genes, thus raising the question of what these target genes are and what their individual functions might be during heart development. To address this question we have utilized RNA-sequencing to compare genome-wide transcriptional expression profiles of flow cytometry-purified mesodermal cells from wild-type, jumu loss-of-function, CHES-1-like loss-of-function, and jumu and CHES-1-like dual loss-of-function embryos. The putative Fkh targets identified by our analysis, i.e. genes exhibiting significant differential expression in jumu and/or CHES-1-like mutants can be divided into four classes: (i) 985 genes that are regulated only by jumu but exhibit no significant change in expression levels in CHES-1-like mutants, (ii) 318 genes that are regulated solely by CHES-1-like, (iii) 287 genes that are differentially expressed both in individual jumu mutants and in CHES-1-like mutants, and (iv) 541 genes exhibiting significantly altered expression levels in embryos lacking both Fkh gene functions, but not in either individual jumu or CHES-1-like loss-of-function mutants, indicating that they are regulated by the two Fkh TFs in a mutually redundant manner. Gene ontology enrichment analyses suggest multiple cardiogenic roles for these putative Fkh targets (specification of cardiac mesoderm, establishment of heart lumen, proper positioning of different heart cell types, sarcomere and myofibril formation, assembly of mitochondrial subunits and processes, cardiac progenitor cell divisions, etc.) that are being experimentally tested.