According to Darwin’s theory, endless evolution leads to a revolution. One such example is the Clustered Regularly Interspaced Palindromic Repeats (CRISPR)–Cas system, an adaptive immunity system in most archaea and many bacteria. Gene editing technology possesses a crucial potential to dramatically impact miscellaneous areas of life, and CRISPR–Cas represents the most suitable strategy. The system has ignited a revolution in the field of genetic engineering. The ease, precision, affordability of this system is akin to a Midas touch for researchers editing genomes. Undoubtedly, the applications of this system are endless. The CRISPR–Cas system is extensively employed in the treatment of infectious and genetic diseases, in metabolic disorders, in curing cancer, in developing sustainable methods for fuel production and chemicals, in improving the quality and quantity of food crops, and thus in catering to global food demands. Future applications of CRISPR–Cas will provide benefits for everyone and will save countless lives. The technology is evolving rapidly; therefore, an overview of continuous improvement is important. In this review, we aim to elucidate the current state of the CRISPR–Cas revolution in a tailor-made format from its discovery to exciting breakthroughs at the application level and further upcoming trends related to opportunities and challenges including ethical concerns.

Melanism in wild felids represents an intriguing evolutionary trait, potentially advantageous under specific ecological conditions, but the genetic basis of this phenotype remains unclear in many populations. Here, we explored melanism in the Indian leopard (Panthera pardus fusca) by integrating whole-genome sequencing with evolutionary and structural analyses. We identified a single-point mutation (p.C117F) in the agouti signalling protein (ASIP) gene. Evolutionary analyses indicated signs of positive selection acting on the ASIP locus, while codon usage patterns revealed no impairment in translational efficiency. Computational predictions (SIFT, PROVEAN) classified the mutation as functionally damaging. Structural modelling combined with molecular dynamics simulations revealed significant disruptions in the stability, helical content, and receptor-binding affinity of the mutated ASIP protein compared to the wild type. The mutation notably diminished ASIP’s inhibitory interaction with melanocortin-1 receptor (MC1R), which is crucial for melanogenesis regulation. Machine-learning models differentiated between mutant and wild-type protein structures by analysing molecular features. Our results support the conclusion that the p.C117F mutation significantly contributes to melanism in Indian leopards, shedding new light on this trait’s molecular underpinnings and evolutionary history. This study identifies the p.C117F mutation as a key driver of melanism in leopards of the Indian subcontinent, providing mechanistic insight into the evolution of complex phenotypes in non-model species.