Body of Abstract: Low oxygen (hypoxia) is the main contributor to plant death during flooding. Anoxia (zero oxygen conditions) is a good approximation of flooding. Calcium ion signaling around the vacuole and its effects on a whole host of hormonal, transcriptional and metabolic factors is a key component of anoxia response. CAXs are vacuolar cation (primarily Ca2+)/proton exchangers. cax1 and cax1/cax3 (DKO) are mutants whose alterations in calcium signaling leads to high levels of anoxia tolerance compared to the wild type (WT). MicroRNAs can modulate stress responses like anoxia such as heat stress, hypoxia etc. Therefore, microRNA libraries were constructed from 3 lines (WT, cax1, DKO) in 2 conditions (pre and post anoxia) repeated thrice from leaf tissue using high throughput sequencing. In the pre-condition, there were no significantly downregulated (50% difference between WT and cax1/dko read counts) microRNAs in the cax1 and DKO. However, there were 51 and 64 significantly upregulated microRNAs in the cax1 and DKO respectively. In the post condition, 22 and 53 microRNAs were upregulated while 2 and 1 microRNAs were downregulated in the cax1 and DKO respectively. Higher numbers of microRNAs relevant to alternative stresses (altitude, hypoxia, ROS, heat) were upregulated in the pre conditions for both DKO and cax1 vs post, indicating that higher expression of stress related microRNAs in the DKO and cax1 predating anoxia may predispose the mutants to superior anoxia tolerance. Several differentially expressed microRNAs in DKO/cax1 pre/post were analyzed through a literature search, which revealed positive roles in hormonally controlled growth suppression and ROS scavenging which may play a role in superior anoxia tolerance. Overall, differential expression of stress related microRNAs along with microRNAs related to growth suppression and ROS scavenging may help explain the superior DKO/cax1 anoxia phenotype.