Salmonella enterica serovar Typhimurium invades the intestinal epithelium using the Salmonella pathogenicity island 1 (SPI1) type III secretion system (T3SS) and induces secretory diarrhea which is still considered a global risk. The regulation of the SPI1 system is controlled by three AraC-like regulators, HilD, HilC and RtsA, that form a feed-forward regulatory loop form, leading to activation of hilA, which encodes the main transcriptional regulators of the T3SS structural genes. Most of the regulatory input is mediated through the translation or stability of the hilD mRNA, or the activity of the HilD protein. The hilD mRNA has an unusual 3’ untranslated region (UTR). The hilD mRNA 3’UTR is 300 nts and can be an independent module that acts as a source of instability for the mRNA. Studies indicated that hilD 3’UTR is regulated by RNase E, the transcriptional terminator Rho, and various small regulatory RNAs (sRNAs). We modified a useful technique to identify the sRNAs that regulates hilD mRNA via the 3’UTR. The technique, which is known as global small non-coding RNA target identification by ligation and sequencing (GRIL-seq), is performed by ligation in vivo of the hilD 3’UTR with any sRNAs that bind through base-pairing and sequencing to identify the chimeric RNAs. Using GRIL-seq, we have identified five novel sRNA that interact with the hilD 3’UTR by base-pairing, resulting in the repression of hilD expression. We also found that the sRNAs act together with Rho and/or RNase E to regulate hilD via the 3’UTR, as the sRNAs lose their regulation in the absence of Rho or RNase E. The use of modified GRIL-seq allows us to identify sRNAs for specific targets in different environments and also helps uncover new roles for these sRNAs.