Visceral Leishmaniasis (VL), also known as kala-azar, is caused by several species of Leishmania, a protozoan parasite (Leishmania donovani) transmitted to humans by the bite of infected phelobotomine argentipes sandflies. VL is a disease of poverty, affecting the poorest of the poor. It is a major cause of morbidity and mortality in some areas (localized). If the infection is left untreated, the patient dies in about 2 years. Several drugs are now available for the treatment of VL. However, some of them are very costly (miltefosine, lipid amphotericin B). Sodium stibogluconate is an effective drug and the backbone of VL treatment for about six decades. Unfortunately, parasites developed resistance against the drug. In some areas in India, for example in North Bihar, approximately 60% of isolates are resistant to this treatment. In addition, the compound exhibits high cardio-toxity, which is an important limiting factor for its use. Based on the new data, which became available, the WHO/SEARO Regional Technical Advisory Group (RTAG) especially constituted for the kala-azar elimination program undertaken by India, Nepal, and Bangladesh in 2005, recommended that miltefosine should be used as the first line drug. However, the RTAG at its meeting in Dhaka (Bangladesh) in 2009 modified the above recommendation and advised that miltefosine should be phased out and replaced by lipid amphotericin B. The decision to switch over to lipid amphotericin B could have been delayed, because the program had already made substantial progress using miltefosine. In view of drug resistance, low compliance, availability and cost, it is imperative that serious efforts should be made to develop new drugs, preferably oral, for the treatment of VL and PKDL.