This study aimed to describe the outcomes of a switch back from DEXi (dexamethasone implant) to anti-VEGF therapy in eyes that were treated temporarily with DEXi after an initial poor response to anti VEGF. Twenty-three eyes of 17 patients were included. These were unresponsive to anti-VEGF and switched to a DEXi after a mean of 12 anti-VEGF injections, and then back to anti- VEGF. The mean age of the cohort at baseline was 68.1 ±8.2 years. The mean duration of diabetes was 19.3 ±9.2 years. The mean time between the last DEXi and the switch back to anti-VEGFs was 4.2 ±1.2 months. The mean best corrected visual acuity (BCVA) increased from 0.25 ±0.19 (decimals) to 0.29 ±0.20 after switching to the DEXi (p=0.11). BCVA remained stable (0.31 ±0.23; p=0.11) after switching back to anti-VEGF, one month after the last injection. The mean central macular thickness (CMT) decreased significantly from 517.0 ±128.5μm to 343.4 ±118.9μm (p<0.001) after switching to the DEXi. In eyes receiving ≥three anti-VEGF injections during the switch back, the CMT one month after the last anti-VEGF injection was significantly decreased compared to the CMT before the switch to the DEXi (a mean change of - 95.55 ±89.82μm, p=0.005). The mean intraocular pressure (IOP) was 17.2 ±3.8 mmHg at baseline, similar to 18.1 ±4.1mmHg two months after the first DEXi (p=0.22) and 18.1 ±4.2mmHg two months after the last DEXi (p=0.84). IOP significantly decreased one month after the last anti-VEGF injection of the switch back (mean IOP 13.3 ±3.6mmHg, p=0.005). The proportion of patients with ocular hypertension (ocular hypertension defined by IOP ≥21mmHg) was 20% at baseline, 13% two months after the first DEXi (p=0.53), 27.3% two months after the last DEXi (p=0.58), and 5.9% one month after the last anti-VEGF injection of the switch back (p=0.21). The conclusion drawn from the study was that switching back poorly responsive eyes to anti-VEGF after temporary DEXi therapy is associated with good anatomical and visual outcomes, provided that at least three anti-VEGF injections are administered. It is speculated that these favourable anatomical outcomes may be due to a “resensitisation of the retinal receptors to anti-VEGFs” by DEXi therapy. A transient use of DEXi may annihilate the effect of pro-inflammatory cytokines, “setting back the counter” to an anti-VEGF-dependent DME. Limitations of the study include limited sample size, retrospective nature and the absence of case-control comparison with eyes pursuing DEXi therapy alone.