The reasons behind the upsurge of mucormycosis cases in India are still unclear. Several factors including use of steroids and other immunomodulators such as tocilizumab, anti-virals, ayurvedic (traditional Indian) medicines especially oils to be instilled in the nose, iron overuse, and use of industrial oxygen have been suggested to play a part. A look at Table 1 however suggests that none of these factors, including steroids and diabetes were uniformly present in the COVID-19 patients presenting with rhino-orbital mucormycosis. Only six out of 13 patients had received oxygen at some point, none had received iron recently, and only one patient had been taking ayurvedic oral medicines (containing Ashwagandha, Withania somnifera). It is quite likely that any of the studied factors such as dysglycaemia might have played only a facilitatory role in triggering mucormycosis cases. We may conclude that COVID-19 has been the primary risk factor for invasive fungal disease. COVID-19 has been observed to increase serum concentrations of GRP78, a heat-shock protein involved in stress-responses. [4] GRP78 has been demonstrated to bind to Rhizopus germlings, which are the major invading forms of Mucorales. [5] Further, antibodies directed against GRP78 and short hairpin RNA (shRNA) sequences targeting GRP78 have been observed to suppress invasion and endothelial damage induced by Rhizopus delemar but not by other pathogenic fungi such as Candia and Aspergillus. [5, 6] Interestingly, anti-GRP78 antibodies have been suggested as potential COVID-19 therapeutic options. [7] This may have a dual effect and may reduce risk of mucormycosis too. A second link between COVID-19 and mucormycosis involves the spleen tyrosine kinase, an enzyme involved in phagocytic function of neutrophils, microphages etc, and hence playing a major role in anti-fungal defense. Urine proteome analysis of COVID-19 patients has shown a down-regulation of spleen-tyrosine kinase, which may impair phagocytosis and predispose to invasive mucormycosis. [8] Paradoxically, Fostamatinib, a small molecule inhibitor of spleen tyrosine kinase, is being tested in clinical trials of COVID-19 patients to improve outcomes by inhibiting pro-inflammatory cytokines and the neutrophil extracellular trap. [9] In contrast to therapies targeting GRP78, this drug may prove to increase the risk of invasive mucormycosis, by inhibiting the phagocytic anti-fungal defense of the body. The interplay of COVID-19 and mucormycosis needs to be worked out based on these pathogenetic pathways in order to adequately prevent the invasive fungal disease with high mortality.